A case-control study of farming and prostate cancer in African-American and Caucasian men

Objective

To determine the risk of prostate cancer associated with farming by duration, recency and specific activities among African‐Americans and Caucasians.

Methods

This population‐based case–control study had information on farming‐related activities for 405 incident prostate cancer cases and 392 controls matched for age, race and region in South Carolina, USA, from 1999 to 2001. Cases with histologically confirmed, primary invasive prostate cancer who were aged between 65 and 79 years were ascertained through the South Carolina Central Cancer Registry. Appropriately matched controls were identified from the Health Care Financing Administration Medicare Beneficiary File. Data were collected using computer‐assisted telephone interviewing, and adjusted odds ratios (aOR) were estimated using unconditional logistic regression.

Results

Farming was associated with increased risk of prostate cancer in Caucasians (aOR 1.8; 95% confidence interval (CI) 1.3 to 2.7) but not in African‐Americans (aOR 1.0; 95% CI 0.6 to 1.6). Regarding specific farming activities, farmers who mixed or applied pesticides had a higher risk of prostate cancer (aOR 1.6; 95% CI 1.2 to 2.2). Increased risk of prostate cancer was observed only for those farming <5 years.

Conclusions

Increased risk of prostate cancer for farmers in this study may be attributable to pesticide exposure. Racial differences in the association between farming and prostate cancer may be explained by different farming activities or different gene–environment interactions by race.Meta‐analyses indicate that farming is more frequently associated with an increased risk of prostate cancer in North America than in other countries.^1,2,3 A total of 8 of 15 studies investigating incidence of prostate cancer in North America found a modestly increased risk among farmers compared with non‐farmers, with effect estimates ranging from 1.1 to 4.3,^{4,5,6,7,8,9,10,11} whereas 7 studies reported no association.^{12,13,14,15,16,17,18} Interestingly, Krstev et al.⁹ found a decreased risk for prostate cancer in farm workers, but an increased risk in those working in agricultural production or with livestock. Studies of mortality from prostate cancer in North America suggest an increase in mortality from prostate cancer among farmers compared with other occupations in 12 of 23 studies, ranging from 1.1 to 1.6.^{19,20,21,22,23,24,25,26,27,28,29,30}Some investigations have assessed prostate cancer risks associated with duration of farming or types of farming (crop, livestock and hay farming, and licensed pesticide application).^{5,6,8,9,10,12,13,16,26,31,32,33} However, only one study assessed prostate cancer risk by farming duration and type of farming among African‐Americans.⁹ Although African‐Americans have the highest incidence of prostate cancer in the world,³⁴ most studies that have evaluated the association between farming and prostate cancer have been carried out on Caucasian men. By contrast, only five studies have reported this association in non‐white men^{24,28,29,35,36} with an even fewer number of investigations in African‐American men.^9,25 Two of these studies had <100 exposed cases in one or both of the racial categories, and one additional study failed to report the number of non‐white cases in farmers. Therefore, we carried out a population‐based case–control study to investigate the risk of prostate cancer among both African‐American and Caucasian farmers using more refined measures of exposure (duration, recency of farming and specific farming‐related activities) while controlling for potential confounders.     

Mortality from Alzheimer's, motor neuron and Parkinson's disease in relation to magnetic field exposure: findings from the study of UK electricity generation and transmission workers, 1973-2004

Background

There are a number of reports linking magnetic field exposure to increased risks of Alzheimer''s disease and motor neuron disease.

Methods

The mortality experienced by a cohort of 83 997 employees of the former Central Electricity Generating Board of England and Wales was investigated for the period 1973–2004. All employees were employed for at least six months with some employment in the period 1973–82. Computerised work histories were available for 79 972 study subjects for the period 1971–93. Information on job and facility (location) were used to estimate exposures to magnetic fields. Two analytical approaches were used to evaluate risks, indirect standardisation (n = 83 997) and Poisson regression (n = 79 972).

Results

Based on serial mortality rates for England and Wales, deaths from Alzheimer''s disease and motor neuron disease were unexceptional. There was an excess of deaths from Parkinson''s disease of borderline significance. No statistically significant trends were shown for risks of any of these diseases to increase with lifetime cumulative exposure to magnetic fields (RR per 10 μT-y: Alzheimer''s disease 1.10 (95% CI 0.90 to 1.33); motor neuron disease 1.06 (95% CI 0.86 to 1.32); Parkinson''s disease 0.88 (95% CI 0.74 to 1.05))

Conclusions

There is no convincing evidence that UK electricity generation and transmission workers have suffered increased risks from neurodegenerative diseases as a consequence of exposure to magnetic fields.A large number of studies have investigated risks of cancer and other diseases in “electrical and electronic” workers. In addition, large-scale cohort mortality studies of electric utility workers that incorporate magnetic field exposure assessments are also available.^1,2,3,4,5 The question has also been raised as to whether employment in “electrical” occupations or exposure to magnetic fields might have an effect on risks of neurodegenerative disease. The literature relating to Alzheimer''s disease and magnetic fields is difficult to assess. It was suggested that increased risks could be substantial.⁶ Although this initial report was based on the combined results of three sub-studies, it should be regarded only as hypothesis forming, as the findings were much influenced by the reclassification of exposure groups. The Alzheimer''s/magnetic fields hypothesis was supported by the findings of another case-control study⁷ and was weakly supported by a proportional mortality ratio analysis of causes of death as recorded on US death certificates.⁸ The hypothesis was not supported, however, by the three studies that were able to provide quantified estimates of individual exposures.^9,10,11 One case-control study⁹ did not show risk to be associated with the individual''s primary occupation, but did show a substantial and statistically significant risk with the last recorded occupation, which would have been the association recorded in the death certificate study.⁸ Neither of the cohort studies,^10,11 however, provided evidence of a risk with increasing exposure, nor, in the one study that provided such information, was there any excess mortality in power plant workers. However, these studies relied on mortality records that are known to under-report Alzheimer''s disease and the distinction between Alzheimer''s disease and dementia is not always clearly made on death certificates. Three more recent studies also provided mixed findings: one providing weak evidence of a risk for males in the highest exposure group,¹² another (overlapping) study focusing on resistance welders showed a positive effect,¹³ and a third study showed an effect in males, but not in females.¹⁴ While initial, hypothesis-generating studies indicated a potential threefold risk, most of the subsequent research has found risks at or below unity, with only a few elevated risks of around 2.0 in selected subgroups. Thus the hypothesis that 50–60 Hz electromagnetic fields (EMFs) increase the risk of Alzheimer''s disease is neither proven nor excluded.More consistent evidence is available for motor neuron disease (some studies are concerned with its principal subtype amyotrophic lateral sclerosis (ALS)).^{8,10,11,12,13,15,16,17,18,19,20,21,22} A number of reports investigating the relation between electrical work or the experience of electrical shocks have been published since the original suggestion was made that electric shocks might increase the risk of the disease.²⁰ Two early studies from Japan (reported in a single paper), where the prevalence both of electrical work (as recorded in medical histories) and electrical shock was low, failed to provide any support for the hypothesis.²¹ However, an increased risk of ALS from electric shocks has been reported in several later studies.^16,22 The US study also found an increased risk associated with the employment in electrical occupations¹⁶ and this was supported by other studies from Sweden¹⁸ and the USA.⁸ Later studies focused on magnetic field exposure^10,11,15 and found twofold risks to be associated with exposure, albeit these excess risks were not always statistically significant. Recent and overlapping studies from Sweden focusing on magnetic field exposure and electric shock are inconsistent, with one showing no effect and the other indicting a twofold risk in the two highest exposure categories.^12,13 The epidemiological evidence suggests that employment in electrical occupations may increase the risk of ALS. However, separating any increased risk as a result of receiving an electric shock from any increased exposure to magnetic fields is important, albeit difficult.A number of epidemiological studies have been carried out on environmental associations with Parkinson''s disease.^{8,10,11,12,13,19,23} No study has provided clear evidence of an association with above average exposures to extremely low frequency EMFs (most risks close to unity) and, in the absence of laboratory evidence to the contrary, it seems unlikely that such exposures are involved in the disease process. Nevertheless, Parkinson''s disease was included as a health outcome of interest in this study for the sake of completeness.This paper seeks to obtain important new information on the topic of occupational magnetic field exposure and risks of mortality from neurodegenerative diseases by examining data from the ongoing epidemiological study of UK electric utility workers; this topic has been identified as a priority in recent reviews.^23,25     

Decline in lung function and mortality: implications for medical monitoring

Aim

To investigate the risk of death associated with selected cut‐off points for rate of decline of forced expiratory volume in one second (FEV₁).

Methods

Mortality rates of a cohort of 1730 coal miners who had performed two pulmonary function tests 12.8 years apart were followed up for an additional 12 years. Based on previous studies, cut‐off points for FEV₁ rate of decline (ml/year) were selected as 30, 60 and 90 ml/year. Cox proportional hazard regression was used to estimate multivariate risk ratio of death in each category.

Results

The risk ratios (compared to “below 30 ml/year”) were 1.39 (95% CI 0.99 to 1.97) in the “60 to less than 90 ml/year” category and 1.90 (95% CI 1.32 to 2.76) in the “90 ml/year and above” category. Rates of decline above 90 ml/year were consistently related to excess mortality. In non‐smokers and those with neither restrictive nor obstructive patterns at the first survey, rates of decline above 60 ml/year were significantly associated with increased mortality.

Conclusions

Risk of death increases in individuals with rates of decline above about 60 ml/year and is statistically significant with declines of 90 ml/year or more. These results should be useful to healthcare providers in assessing lung function declines observed in individuals.Pulmonary function has been recognised as an important predictor of mortality.^{1,2,3,4,5,6,7,8,9,10} Studies have conclusively demonstrated that the level of pulmonary function, measured using various functional parameters, is inversely associated with subsequent mortality from all causes, lung cancer and cardiovascular disease.^{1,2,3,4,5,6,7,8,9,10} Additionally, an association between the rate of decline in lung function and both cardiovascular and all‐cause mortality has been observed in several studies.^{11,12,13,14,15} Although previous studies have shown an association between rate of decline and mortality,^12,13,14,15 they did not define the degree of mortality risk associated with categories of rates of decline that may be useful in screening for respiratory impairment and preventing lung disease. Such risk information may be helpful in guiding the interpretation of lung function decline in relation to the risk of impairment, disability and, ultimately, death. When monitoring lung health, the rate of pulmonary function decline in an individual provides information that can be used for triggering interventions before an individual develops irreversible respiratory impairment and disability. The question addressed in this study is: what rate of sustained forced expiratory volume in one second (FEV₁) decline indicates a significant risk for death? In healthy adults, FEV₁ declines on average between 25 and 30 ml/year as part of the normal aging process.¹⁶ Mean FEV₁ declines of 60 ml/year, double the rate in healthy individuals, have often been observed in cigarette smokers,^17,18 while declines greater than 90 ml/year, or triple what is expected, may be seen in susceptible individuals who progress to chronic obstructive pulmonary disease (COPD).¹⁹ Rate of FEV₁ decline cut‐off points, such as 60 ml/year and 90 ml/year could be considered clinical benchmarks.The aim of this study is to further investigate in a male working population the relation between rates of decline in pulmonary function and subsequent mortality, and to quantify the excessive mortality risk associated with different categories of decline considered important in clinical practice and research.     

Short-term effects of ozone air pollution on ischaemic stroke occurrence: a case-crossover analysis from a 10-year population-based study in Dijon, France

Objective

To evaluate the association between air pollutants and the occurrence of acute stroke from 10‐year population‐based study.

Methods

The daily stroke count was obtained from Dijon Stroke Register between March 1994 and December 2004. The register recorded all first‐ever strokes among residents of Dijon (150 000 inhabitants) in France, using standard diagnostic criteria. Pollutant concentrations (SO₂, CO, NO_2, O₃ and PM₁₀) were measured hourly. A bi‐directional case‐crossover design was used to examine the association between air pollutant and stroke onset. The conditional logistic regression model included the meteorological parameters (temperature, relative humidity), influenza epidemics and holidays.

Results

The authors collected 493 large artery infarcts, 397 small artery infarcts, 530 cardio‐embolic infarcts, 67 undeterminate infarcts, 371 transient ischaemic attacks and 220 haemorrhagic strokes. For single‐pollutant model and for a 10 mg/m³ increase of O₃ exposure, a positive association was observed only in men, over 40 years of age, between ischaemic stroke occurrence and O₃ levels with 1‐day lag, (OR 1.133, 95% CI 1.052 to 1.220) and 0‐day lag (OR 1.058, 95% CI 0.987 to 1.134). No significant associations were found for haemorrhagic stroke. In two‐pollutant models, the effects of O₃ remained significant after each of the other pollutants were included in the model, in particular with PM₁₀. A significant association was observed for ischaemic strokes of large arteries (p = 0.02) and for transient ischaemic attacks (p = 0.01). Moreover, the authors found an exposure‐response relations between O₃ exposure and ischaemic stroke (test for trend, p = 0.01). An increase in association in men with several cardiovascular risk factors (smoker, dyslipidemia and hypertension) was also observed.

Conclusion

These observational data argue for an association between ischaemic stroke occurrence and O₃ pollution levels; these results still need to be confirmed by other studies.Numerous epidemiological studies have shown the potential deleterious effects of ambient air pollution on health.^{1,2,3,4,5,6,7,8,9,10} Consequences have been clearly described in terms of cardiovascular mortality and morbidity.^{1,2,3,4,5,6,7,8,9,10,11} Several pathophysiological hypotheses have been suggested to explain the increased risk of cardiovascular diseases including effects on blood coagulation, endothelial dysfunction, systemic inflammatory responses, acute arterial vasoconstrictions or a propensity for arrhythmias.¹¹ Consequences of these effects may be alterations of atheromatous plaque, enhanced potential for acute thrombosis or acceleration of the progression of atherosclerosis.¹¹ It is reasonable to hypothesise that similar consequences might exist for strokes. However, little is known about occurrence of stroke in relation to air pollution. A few recent studies have reported an association between stroke mortality and pollution.^12,13,14,15 However, the significant relative risks observed were weak and one study failed to confirm the association.⁴ Furthermore with mortality indicators, we do not know whether air pollution is a causative factor of stroke occurrence or only a precipitating factor of death after stroke, because data are analysed with the date of death rather than that of stroke onset. The studies looking into an association between hospital admissions for stroke and air pollution also generated conflicting results: some studies point to an association,^6,16,17,18 and others do not.^2,4,19,20 Lastly, the indicators used in these studies (mortality, hospital admission) may be sources of specific biases.²¹ For these reasons, these previous results must be confirmed thoroughly.For this study, we hypothesise that air pollutants may have significant effects on stroke onset. To examine the nature of this relation, we used morbidity indicators from a population‐based register in Dijon, France. The aim of the study was to investigate the relation in the short term between urban air pollution and stroke incidence.     

Risk factors for new episodes of sick leave due to neck or back pain in a working population. A prospective study with an 18-month and a three-year follow-up

Objectives

To identify risk factors for new episodes of sick leave due to neck or back pain.

Methods

This prospective study comprised an industrial population of 2187 employees who were followed up at 18 months and 3 years after a comprehensive baseline measurement. The potential risk factors comprised physical and psychosocial work factors, health‐related and pain‐related characteristics and lifestyle and demographic factors. The response rate at both follow‐ups was close to 73%.

Results

At the 18‐month follow‐up, 151 participants reported at least one episode of sick‐listing due to neck or back pain during the previous year. Risk factors assessed at baseline for sick leave due to neck or back pain at the follow‐up were blue‐collar work, back pain one or several times during the previous year, 1–99 days of cumulative sickness absence during the previous year (all causes except neck or back pain), uncertainty of one''s own working ability in 2 years'' time and the experience of few positive challenges at work. After 3 years, 127 participants reported at least one episode of sick leave due to back or neck pain during the year previous to follow‐up. The risk factors for this pain‐related sick leave were blue‐collar work, several earlier episodes of neck pain, no everyday physical activities during leisure time (cleaning, gardening and so on), lower physical functioning and, for blue‐collar workers separately, repetitive work procedures.

Conclusion

The most consistent risk factors for new episodes of sick leave due to neck or back pain found during both the follow‐ups were blue‐collar work and several earlier episodes of neck or back pain assessed at baseline. Preventive efforts to decrease sick leave due to neck or back pain may include measures to increase the occurrence of positive challenges at work and to minimise repetitive work procedures. An evidence‐based secondary prevention of neck and back pain including advice to stay active is also warranted.Lower back and neck pain have a high prevalence and incidence in adult populations,¹ and social expenditure due to these ailments is huge.² Indirect costs such as sickness absenteeism and disability pensions constitute approximately 90% of this expenditure.³ Well‐designed longitudinal studies have been called for to assess factors related to sick leave, including risk factors for being sick‐listed.⁴A large body of research has been aimed at discerning risk factors for developing neck or back pain and/or chronic disability and several reviews have summarised these findings. On the whole, it seems that the physical load at work—for example, manual material handling, bending and twisting and whole‐body vibrations—increases the risk for back pain.^5,6 With regard to psychosocial factors in the workplace, some authors have concluded that, among other things, low job satisfaction and low social support^7,8 are related to the onset of back pain; whereas other researchers have found moderate evidence for no relation between back pain and psychosocial factors at work.⁹ Furthermore, psychological factors such as distress and depressed mood have been related to new episodes of neck or back pain¹⁰ and subsequent chronicity or disability.¹¹ Regarding life‐style factors, some evidence indicates that smoking may be related to back pain^12,13 even though this has not been confirmed in all studies.¹⁴ Physical activity, or inactivity, during leisure time has not been consistently related to the occurrence of back pain.^5,15Most people will experience one or more episode(s) of neck or back pain during their lives,¹ but only a small proportion will seek help and/or become sick‐listed because of these complaints.^16,17 Therefore, it seems reasonable to assume that sick leave due to neck or back pain is predicted by different factors other than those predicting the onset of neck or back pain.^14,18A number of studies have examined factors related to future sick leave due to neck or back pain; however, in a recent systematic review it was concluded that there is only limited evidence that certain work‐related characteristics, together with a few medical/functional factors and some demographic factors, are risk factors for future sick‐listing due to back or neck pain.¹⁹ Physical and/or ergonomic factors such as troublesome working postures and/or heavy lifting have been reported in some studies to increase the risk of future sick leave due to neck or back pain,^{14,20,21,22,23} but they were not related to sick‐listing in other studies.^24,25,26 Psychosocial factors in the work environment have also emerged as predictors of sick listing. These include low job satisfaction,^23,24,26 low control over work and a low work pace among men²⁷; low decision‐making authority and medium skill discretion²⁰ and low coworker support.^14,26 However, in a study by Elders et al,²¹ psychosocial work characteristics were not related to sickness absence due to back pain.Factors such as pain intensity,^21,22 reports of earlier episodes of back pain,^22,27 results from the straight‐leg‐raising test and medical history,²⁴ sick‐listing in general,²⁸ demographics/background such as age,²⁹ employment grade,²⁷ working night shifts²² and a few others such as emotional distress or low mood,^24,30 disability²⁶ and heavy smoking¹⁴ have also predicted sick‐listing attributed to back pain. However, divergent results have been found in other studies—for example, age, earlier back pain and smoking were not found to predict sick leave due to back pain in a study by Burdorf et al.³¹A better knowledge of factors related to future sick leave attributable to neck or back pain could be instrumental in decision‐making regarding preventive measures aimed at reducing sickness absence due to these conditions. The aim of this prospective study was to identify factors that predict new episodes of sick leave attributed to neck or back pain in an occupational population.     

The validation of work-related self-reported asthma exacerbation

Objective

To determine the validity of work‐related self‐reported exacerbation of asthma using the findings from serial peak expiratory flow (PEF) measurements as the standard.

Methods

Adults with asthma treated in a health maintenance organisation were asked to conduct serial spirometry testing at home and at work for 3 weeks. Self‐reported respiratory symptoms and medication use were recorded in two ways: a daily log completed concurrently with the serial PEF testing and a telephone questionnaire administered after the PEF testing. Three researchers evaluated the serial PEF records and judged whether a work relationship was evident.

Results

95 of 382 (25%) working adults with asthma provided adequate serial PEF data, and 13 of 95 (14%) were judged to have workplace exacerbation of asthma (WEA) based on these data. Self‐reported concurrent medication use was the most valid single operational definition, with a sensitivity of 62% and a specificity of 65%.

Conclusions

A work‐related pattern of self‐reported asthma symptoms or medication use was usually not corroborated by serial PEF testing and failed to identify many people who had evidence of WEA based on the serial PEF measurements.Work‐related asthma (WRA)is the most common non‐asbestos related occupational respiratory disease in the US and in most industrialised nations.^1,2,3,4 It accounts for about 25% of all reported occupational lung diseases in the UK⁵ and an estimated 15% of asthma cases in the US are work related.^4,6,7,8 In the US, the Sentinel Event Notification System for Occupational Risks (SENSOR) case‐classification scheme for WRA encompasses both new‐onset asthma and work‐aggravated asthma.⁹ Work‐aggravated asthma is defined as the aggravation or exacerbation of pre‐existing asthma due to occupational exposures. Based on SENSOR data of four states from 1993 to 1995, 19.1% of WRA cases were in the aggravation category.⁹ These cases had similar adverse outcomes as the new‐onset cases, such as persistent breathing problems and the need for emergency care.¹⁰Questionnaires that gather information on symptoms and exposures are frequently used to assess WRA.¹¹ Questionnaires are inexpensive and feasible for large population‐based studies, but patients must be able to clearly perceive their respiratory status for their responses to be useful. Unfortunately, asthma patients'' perceptions of dyspnoea are not always consistent with measured levels of air flow obstruction.¹² One study showed that 15% of people with asthma failed to be aware of any discomfort after a 20% reduction in their forced expiratory volume in one second.¹³ The inability of a patient to accurately perceive substantial changes in his or her lung function results in inaccurate reporting of symptoms due to either blunted perception or over perception.¹⁴ Therefore, self‐reported symptoms could not be effective surrogates for more objective diagnostic tools in determining the contribution of exposures at work to the onset or exacerbation of asthma.Serial measurements of peak expiratory flow (PEF) are an established objective aid in the diagnosis of WRA.^15,16 The test allows for simple, inexpensive measurement of lung function outside of a clinic or laboratory.^15,17,18,19 Serial PEF measurements have a high sensitivity and even higher specificity for WRA.^19,20,21 For example, when using specific inhalation challenges as the standard for occupational asthma, serial PEF measurements were found to have a sensitivity of 70–75% and a specificity of 94–100%.^20,21The primary objective of this investigation was to validate work‐related self‐reported exacerbation of asthma using the findings from serial PEF measurements as the standard.     

Air pollution and inflammation in type 2 diabetes: a mechanism for susceptibility

Background

Particulate air pollution has been associated with several adverse cardiovascular health outcomes, and people with diabetes may be especially vulnerable. One potential pathway is inflammation and endothelial dysfunction—processes in which cell adhesion molecules and inflammatory markers play important roles.

Aim

To examine whether plasma levels of soluble intercellular adhesion molecule 1 (ICAM‐1), vascular cell adhesion molecule 1 (VCAM‐1) and von Willebrand factor (vWF) were associated with particle exposure in 92 Boston area residents with type 2 diabetes.

Methods

Daily average ambient levels of air pollution (fine particles (PM_2.5), black carbon (BC) and sulphates) were measured approximately 500 m from the patient examination site and evaluated for associations with ICAM‐1, VCAM‐1 and vWF. Linear regressions were fit to plasma levels of ICAM‐1, VCAM‐1 and vWF, with the particulate pollutant index, apparent temperature, season, age, race, sex, glycosylated haemoglobin, cholesterol, smoking history and body mass index as predictors.

Results

Air pollutant exposure measures showed consistently positive point estimates of association with the inflammatory markers. Among participants not taking statins and those with a history of smoking, associations between PM_2.5, BC and VCAM‐1 were particularly strong.

Conclusions

These results corroborate evidence suggesting that inflammatory mechanisms may explain the increased risk of air pollution‐associated cardiovascular events among those with diabetes.Outdoor air quality standards worldwide are intended to protect the most sensitive people in the population, yet studies linking outdoor pollution and health have observed associations even at pollutant levels well below the standards.^1,2 One important regulated pollutant is particles <2.5 μm in aerodynamic diameter (PM_2.5), formed as a result of fossil‐fuel combustion by motor vehicles and stationary sources such as power plants. These fine particles are of concern for health as they can deposit in the lower airways and gas‐exchanging portions of the lung, even reaching the circulatory system.³ Exposure to increased levels of outdoor particulate air pollution has been consistently linked to cardiovascular morbidity and mortality, and to changes in subclinical indicators of cardiovascular function.⁴ Inflammation due to oxidative stress may be one responsible mechanism,⁴ as suggested by both animal and human studies.^5,6,7Individuals with diabetes are at greater risk of dying⁸ and being hospitalised for heart disease⁹ during periods of high air pollution. Long‐term exposure to PM_2.5 was associated with a higher relative risk of mortality among people with diabetes compared with the general population.¹⁰ Hence, those with diabetes may be considered a sensitive population. Examining the potential biological mechanisms responsible for this enhanced susceptibility, and identifying specific air pollution sources that may be more toxic, is therefore a priority for researchers and policy makers.⁴ Obesity is prevalent among people with diabetes and involves an increased inflammatory burden, thus lending plausibility to the idea that inflammation is involved in sensitivity to the cardiovascular effects of particles.^11,12Inflammation is a key pathway leading to atherosclerosis and subsequent adverse cardiovascular events,¹³ and several blood markers of inflammation are being evaluated for their ability to predict prevalent or incident cardiovascular disease. These include the intercellular adhesion molecule 1 (ICAM‐1) and the vascular cell adhesion molecule 1 (VCAM‐1), which are expressed on cell surfaces and are also found, in soluble form, in the plasma.¹⁴ Another inflammatory marker is von Willebrand factor (vWF): a polypeptide involved in the thrombotic pathway, and a marker of endothelial damage or dysfunction.¹⁵ Increased plasma levels of soluble ICAM‐1 and VCAM‐1, and vWF have been associated with inflammatory, cardiovascular and neoplastic disease outcomes,^{14,15,16,17,18,19,20,21} although VCAM‐1 associations have been less consistent than for ICAM‐1.^17,18,22 Prospective studies have linked vWF with risk of heart attack and coronary heart disease.^16,23 Increased levels of vWF and soluble VCAM‐1 and ICAM‐1 are also associated with diabetes prevalence,^24,25 and higher VCAM‐1 and ICAM‐1 levels are associated with development of type 2 diabetes and its complications.^25,26A few toxicological and epidemiological studies have examined the associations between ICAM‐1, VCAM‐1, and/or vWF levels and particle exposures,^{27,28,29,30,31,32,33} but none focused specifically on individuals with diabetes. Previously, we evaluated impaired vascular reactivity as one potential mechanism for increased sensitivity to particle‐mediated health effects.³⁴ This study examines whether ambient levels of airborne particles are associated with inflammation, as marked by increased ICAM‐1, VCAM‐1 and vWF plasma levels, among people with diabetes residing in metropolitan Boston, Massachusetts, USA.     

Potential of ultrasonography for epidemiological study of work-related wrist tenosynovitis

Objective

To explore the possible role of ultrasonography in case definitions for epidemiological studies of work‐related wrist tenosynovitis.

Methods

Clinical and ultrasonography (7.5 MHz linear probe) data systematically collected from meat workers (n = 128) with biomechanical exposure characterisation were analysed. The diagnostic accuracy of different combinations of potentially relevant ultrasonography findings (nonhomogeneity, thickening and anechoic halo) was evaluated using symptomatology as a reference standard. The concordance between ultrasonography findings and symptoms was then analysed.

Results

Analysis of wrist biomechanical exposure was suggestive of increased prevalence of musculoskeletal disorders. Using symptoms as a reference standard, each of the three ultrasonography findings (and their combinations) showed good specificity (⩾85%) accompanied by low sensitivity (<60%); the positive likelihood ratio for at least two findings was 4.1. κ Values (95% confidence intervals) between symptoms and different sets of ultrasonography findings were as follows: for non‐homogeneity, κ = 0.31 (0.19 to 0.43); at least one finding, κ = 0.28 (0.16 to 0.40); at least two findings, κ = 0.32 (0.20 to 0.44); all p<0.01.

Conclusion

The use of ultrasonography in symptomatic subjects could contribute to a more specific epidemiological case definition of wrist tenosynovitis. The results of this study could help orient future research in this direction.Tenosynovitis of the wrist (also known as wrist tendinopathy or wrist tendinitis) commonly accompanies forceful and repetitive wrist–hand activities, especially when associated with awkward wrist posture. Epidemiological studies of wrist tenosynovitis commonly use clinical case definitions based on symptoms, sometimes in conjunction with physical signs and clinical history.^{1,2,3,4,5,6,7,8,9} Results can be affected by the choice of case definition and the validity of the diagnostic techniques.¹⁰ However, the symptoms and physical signs associated with the wrist are not specific, and further investigation is needed to form a reliable case definition for epidemiological studies.^{11,12,13,14,15}Portable high‐resolution (7–15 MHz) ultrasound transducers allow dynamic examination of tendons and can provide a rapid, relatively inexpensive non‐invasive imaging tool suitable for epidemiological studies. Ultrasonography is now an elective means to study tendons, sheaths and many of their pathological changes (infective, rheumatic or traumatic inflammation; partial or entire ruptures; effects of diabetes and other degenerative disorders).^16,17,18 However, the role of ultrasonography in the epidemiological classification of overuse tenosynovitis, including acute and degenerative changes, is yet to be clearly defined.To investigate the possible role of high‐resolution ultrasonography in case definitions for epidemiological studies of wrist tenosynovitis, we analysed data collected for this purpose from a population of meat workers highly exposed to biomechanical risk factors. We first used the presence of symptoms as a reference standard for assessing the diagnostic accuracy of selected ultrasonography findings. As symptomatology cannot be considered a diagnostic gold standard, we also analysed the concordance of ultrasonography findings with symptoms.     

Heat‐related and cold‐related deaths in England and Wales: who is at risk?

Background

Despite the high burden from exposure to both hot and cold weather each year in England and Wales, there has been relatively little investigation on who is most at risk, resulting in uncertainties in informing government interventions.

Objective

To determine the subgroups of the population that are most vulnerable to heat‐related and cold‐related mortality.

Methods

Ecological time‐series study of daily mortality in all regions of England and Wales between 1993 and 2003, with postcode linkage of individual deaths to a UK database of all care and nursing homes, and 2001 UK census small‐area indicators.

Results

A risk of mortality was observed for both heat and cold exposure in all regions, with the strongest heat effects in London and strongest cold effects in the Eastern region. For all regions, a mean relative risk of 1.03 (95% confidence interval (CI) 1.02 to 1.03) was estimated per degree increase above the heat threshold, defined as the 95th centile of the temperature distribution in each region, and 1.06 (95% CI 1.05 to 1.06) per degree decrease below the cold threshold (set at the 5th centile). Elderly people, particularly those in nursing and care homes, were most vulnerable. The greatest risk of heat mortality was observed for respiratory and external causes, and in women, which remained after control for age. Vulnerability to either heat or cold was not modified by deprivation, except in rural populations where cold effects were slightly stronger in more deprived areas.

Conclusions

Interventions to reduce vulnerability to both hot and cold weather should target all elderly people. Specific interventions should also be developed for people in nursing and care homes as heat illness is easily preventable.The large death toll and disruption associated with the bitterly cold weather in Central and Eastern Europe in the winter of 2005–6 was a timely reminder of how poorly prepared many populations are to the dangers of extreme cold temperatures (http://news.bbc.co.uk/1/hi/world/europe/4643718.stm). Similarly, the dangers of hot weather were shown dramatically by the 2003 heat wave that accounted for >30 000 deaths throughout western Europe,¹ and >2000 deaths in England and Wales alone.²Health protection measures are being increasingly developed. The Department of Health''s heatwave plan for England was implemented rapidly in 2004 and includes monitoring of health surveillance data.³ Measures to prevent cold‐related mortality currently focus on activities to reduce fuel poverty and improve home insulation,⁴ as well as advise about behaviour when outdoors.⁵ However, many uncertainties remain in the identification of those most vulnerable to both hot and cold weather and the most effective means of health protection.Excess winter mortality in the UK, although falling, is higher than in other European countries.⁶ Some of this high winter burden can be explained by behavioural factors reflecting poor adaptation to cold weather,^7,8 and poorly insulated housing also has a key role.⁴ It has been observed that winter mortality can be higher among lower social classes^9,10; however many others have observed no association with deprivation in the UK,^{11,12,13,14,15,16,17} which is consistent with poorly heated homes being more prevalent in the middle classes.Information from heatwave events in the US and Europe suggests that vulnerability to heat can be modified by intrinsic factors such as age,² sex^18,19 and possibly race.²⁰ Other “acquired” characteristics may also predispose individuals to heightened susceptibility to environmental exposures.²¹ These include pre‐existing medical conditions such as cardiorespiratory diseases, neurological diseases and mental illness.¹⁹As with cold, the evidence for whether effects of heat are modified by socioeconomic status is unclear. Studies from the US have observed an association with deprivation,^{22,23,24,25,26} where lack of air conditioning is a strong marker for poverty. However, other work, using area‐level indicators, observed no modification of the heat effect in Sao Paulo.²⁷ Other contextual characteristics that increase susceptibility to heat exposure are social isolation,^28,29 living in urban areas³⁰ and living on the top floors of buildings.³¹ Many deaths in France during the 2003 heat wave occurred in nursing and residential homes.³² Important differences in heatwave mortality were also reported between cities in Europe.¹ The population in the northern part of France, away from the Atlantic coast, was most affected.³³By using long time‐series datasets of daily mortality counts for each region of England and Wales, we investigated which subgroups of people are most at risk from exposure to hot and to cold weather. Risk factors were identified by linkage of mortality files to small area‐level variables on the 2001 UK census and to a database of all care and nursing homes to determine whether or not individuals were residents of care homes at the time of death.     

The effect of individual counselling and education on work ability and disability pension: a prospective intervention study in the construction industry

Objectives

To investigate the effectiveness of a counselling and education programme on work ability and work disability pension for employees in the construction industry.

Methods

Employees with a high disability risk of 38% or more in the following four years were included. Employees in the intervention group were either selected by an occupational physician or enrolled themselves. They received an assessment and individual programme focused on optimising work functioning, while the control group received care-as-usual. Data on work ability measured with the Work Ability Index (WAI) and work disability pensions were collected at baseline during a periodic occupational health examination and at 9, 18 and 26 months after the start of the intervention using a questionnaire.

Results

Most employees in both the intervention (n = 83) and control group (n = 209) were carpenters (43% and 37%) and bricklayers (7% and 15%). In the intervention group, 42% successfully completed the programme. Work ability in the intervention group was lower at baseline but showed an increase over time while work ability of the control group remained the same. The work ability in the intervention group improved slightly more (p = 0.09). No statistically significant differences in percentages of employees receiving a disability pension between the intervention and control group were found at 9 or 18 months and no differences in the age-adjusted percentages of employees receiving a disability pension were found between the groups at any measurement.

Conclusions

The programme was slightly effective in improving the work ability but not in reducing work disability pensions. A more comprehensive multidisciplinary intervention programme might be necessary.Workers in the construction industry are often exposed to hazardous working conditions, including the manual handling of loads, and exposure to vibration, noise, dust and chemicals.^1,2 Adverse mental work conditions such as working under time pressure, employment without security or having boring work are also prevalent.³ It is, therefore, well recognised that construction workers are at a greater risk of developing health disorders and associated disabilities than workers in other industries and the general population.^1,4,5 Several studies in Europe and the USA found that construction employees had a higher prevalence of musculoskeletal disorders, nervous complaints, allergies, lung diseases and hearing deficiencies.^3,5,6,7 Moreover, accidents and falls are very common in the construction industry^8,9 and they can result in serious injuries.Among construction workers these health problems caused by the sustained heavy physical and/or mental working load, in addition to frequent accidents and injuries, are likely to reduce their work capacities and may lead to temporary absence from work and ultimately to permanent disability. A number of studies in European countries have shown a high incidence of permanent work incapacity among construction workers,^4,10 mainly from musculoskeletal and cardiovascular diseases.^1,4It is important to prevent work disability pension because of the human and societal costs. Prevention of early retirement as a result of disability will become even more important, because the number of construction workers at risk for early retirement on health grounds is likely to rise in the near future as a result of the ageing population and work force.³ At the same time, recent changes in the social legislation in Europe^3,11,12 and the recognition of disability pensioning as a social problem^1,12 may imply that workers need to retire later than they have done in recent years.In order to support workers at risk for a work-related disability in their efforts to remain in paid employment, early intervention programmes are needed that increase the work ability of workers whose capabilities at work no longer match the physical or mental requirements of their jobs. However, few such early intervention programmes for workers in the construction industry or elsewhere exist.^13,14 It has been hypothesised that active management and coaching of the individual employee with difficulties prolonging his or her working life could prevent the construction worker at risk from early retirement by improving his work ability.^15,16 Therefore, an intervention programme adopted on the individual capacities and focused on optimising work functioning was created for the construction industry. It was based on individual counselling, education and coaching in the workplace and/or support.The aim of this study was to evaluate whether this occupational health intervention programme for construction workers at risk could (1) increase work ability and (2) reduce work disability pensions.     

Association of low blood pressure with anxiety and depression: the Nord-Trøndelag Health Study

Background

Low blood pressure has mainly been regarded as ideal, but recent studies have indicated an association with depression in elderly people.

Objective

To investigate whether low blood pressure is associated with anxiety and depression in the general population.

Design

Cross‐sectional study.

Setting

Participants in the population‐based Nord‐Trøndelag Health Study (HUNT‐2, 1995–7), Norway.

Participants

60 799 men and women aged 20–89 years filled in the Hospital Anxiety and Depression Scale as part of a general health study. Systolic and diastolic blood pressure was classified in age‐stratified and sex‐stratified centile groups.

Main results

Compared with participants with systolic blood pressure within the 41–60 centile (reference) group, the odds ratio for anxiety was 1.31 (95% confidence intervals (CI) 1.16 to 1.49), for depression 1.22 (95% CI 1.03 to 1.46), and for comorbid anxiety and depression 1.44 (95% CI 1.24 to 1.68) in the group with ⩽5 centile systolic blood pressure. Slightly weaker associations were found of low diastolic blood pressure with anxiety and depression. These associations were similar across sex and age groups. Physical impairment, smoking and angina pectoris influenced the associations only marginally, whereas stroke, myocardial infarction, use of drugs for hypertension, body mass index and several other covariates had no influence.

Conclusions

This study represents epidemiological evidence for an association of low blood pressure with anxiety and depression, which is not caused by cardiovascular disease.The global burden of hypertension as a leading risk factor for cardiovascular and kidney disease, and for mortality,¹ has overshadowed possible health problems associated with chronic low blood pressure. Through decades, medicine has viewed hypotension as an ideal blood pressure level,² and as an example of a non‐disease.³ Earlier, however, low blood pressure was associated with neurasthenic symptoms such as tiredness, weakness, dizziness and headache,⁴ and with sleep disturbances, anxiety and depression.⁵ Although chronic low blood pressure can still be used in some continental European countries to explain a variety of constitutional symptoms, the prevailing attitude in English‐speaking countries has been that low blood pressure does not produce symptoms.^5,6Psychosomatic research on blood pressure has mainly focused on hypertension.^7,8,9 Several studies have indicated an association between hypertension and psychological factors. However, the psychometric properties of the scales used have often been less well established,⁹ and most previous studies have not explored the lower range of blood pressure. By contrast, some studies have indicated that low blood pressure is associated with various somatic and psychological symptoms.^5,10,11,12 Four of six geriatric studies, using standardised screening inventories for depression, found an association between low blood pressure and depression,^6,13,14,15 one study found no association,¹⁶ whereas a recent study found an association between hypertension and depression.¹⁷ However, the design and findings in some of the studies have been contested.¹⁸ In the absence of a commonly accepted definition of low blood pressure, various boundaries have been used. Four geriatric studies defined blood pressure <120/75 mm Hg as hypotensive, 120–139/75–84 mm Hg as normal and ⩾140/85 mm Hg as hypertensive.^6,13,15,16As most previous studies have limitations, and as their results are inconsistent, we wanted to examine the association of blood pressure with anxiety and depression in the general population using a standardised screening inventory. Our large sample size and broad age range gave an opportunity to explore both tails of the blood pressure distribution, and to control for body weight, cigarette smoking, cardiovascular disease and other relevant covariates.     

Comparison of two indices of exposure to polycyclic aromatic hydrocarbons in a retrospective aluminium smelter cohort

Background

The association between coal tar‐derived substances, a complex mixture of polycyclic aromatic hydrocarbons, and cancer is well established. However, the specific aetiological agents are unknown.

Objective

To compare the dose–response relationships for two common measures of coal tar‐derived substances, benzene‐soluble material (BSM) and benzo(a)pyrene (BaP), and to evaluate which among these is more strongly related to the health outcomes.

Methods

The study population consisted of 6423 men with ⩾3 years of work experience at an aluminium smelter (1954–97). Three health outcomes identified from national mortality and cancer databases were evaluated: incidence of bladder cancer (n = 90), incidence of lung cancer (n = 147) and mortality due to acute myocardial infarction (AMI, n = 184). The shape, magnitude and precision of the dose–response relationships and cumulative exposure levels for BSM and BaP were evaluated. Two model structures were assessed, where 1n(relative risk) increased with cumulative exposure (log‐linear model) or with log‐transformed cumulative exposure (log–log model).

Results

The BaP and BSM cumulative exposure metrics were highly correlated (r = 0.94). The increase in model precision using BaP over BSM was 14% for bladder cancer and 5% for lung cancer; no difference was observed for AMI. The log‐linear BaP model provided the best fit for bladder cancer. The log–log dose–response models, where risk of disease plateaus at high exposure levels, were the best‐fitting models for lung cancer and AMI.

Conclusion

BaP and BSM were both strongly associated with bladder and lung cancer and modestly associated with AMI. Similar conclusions regarding the associations could be made regardless of the exposure metric.The primary exposure of aluminium smelting cohort to coal tar‐derived substances has been associated with increased risk of bladder and lung cancer.^{1,2,3,4,5,6,7,8} Coal tar‐derived substances are a complex mixture that includes over 100 polycyclic aromatic hydrocarbons (PAHs), several of which are known carcinogens.^9,10 The mixture may also contain very low levels of amino‐PAHs and nitro‐PAHs, which are also known bladder carcinogens.^11,12 Exposure to PAHs has also been associated with cardiovascular disease mortality within aluminium smelter cohorts and within other industries with PAH exposure,^6,13 but only a recent study of male asphalt workers has demonstrated a consistent dose–response relationship.¹⁴ Although PAHs are suspected, the specific causal agents of the increased risk of cancer and cardiovascular disease in aluminium smelters are not known.^{9,14,15,16,17}The occurrence of exposure to PAHs as a mixture creates significant challenges for exposure assessment in epidemiological studies. One challenge is in choosing an appropriate indicator of the carcinogenic or toxic potential of the mixture. Epidemiological studies have used various indicators, including measurements of individual hydrocarbons of the mixture, to describe exposure to PAHs and to examine dose–response relationships. These measures have included benzene‐soluble materials (BSMs), total particulate PAHs and benzo(a)pyrene (BaP), owing to routine monitoring of these components at most smelters.¹⁸ Of these metrics, BaP has been proposed to be a more specific indicator of exposure to PAHs as a class of carcinogens, and thus a better indicator of the carcinogenic potential of coal tar‐derived substances than BSM.^16,17 Initial comparisons between BaP and BSM as exposure indices in aluminium smelter studies have found that BaP provided a slight improvement in the dose–response relationship for bladder cancer,^3,17 whereas BSM provided a better‐fitting dose–response relationship for lung cancer.²A recent follow‐up health study at a vertical stud Söderberg aluminium smelter provided an opportunity to compare exposure indices of BSM and BaP quantitatively in analyses of mortality and cancer incidence. In contrast with other aluminium smelter studies that used the work‐area‐specific relationship between BaP and BSM to derive estimates of exposure to BaP,^2,3 the BaP exposure index used here was derived independently of BSM exposure levels.¹⁹ In this study, our objective was to examine the dose–response relationships to determine which of the exposure indices, BSM or BaP, provided a better marker for the causal component(s) of coal tar‐derived substances. The shape of the dose–response relationship was examined using both a log‐linear model (ln(relative risk (RR)) = β*cumulative exposure) and a log–log model (ln(RR) = β*ln(cumulative exposure+1)) structure. The focus of the dose–response relationships presented in this paper was on bladder cancer incidence, lung cancer incidence, and mortality due to AMI, because a substantial number of cases were available for examining the slope of dose–response relationships and monotonically increasing risks have been observed in categorical analyses.¹     

Road traffic noise and hypertension

Background

It has been suggested that noise exposure increases the risk of hypertension. Road traffic is the dominant source of community noise exposure.

Objective

To study the association between exposure to residential road traffic noise and hypertension in an urban municipality.

Methods

The study population comprised randomly selected subjects aged 19–80 years. A postal questionnaire provided information on individual characteristics, including diagnosis of hypertension. The response rate was 77%, resulting in a study population of 667 subjects. The outdoor equivalent traffic noise level (Leq 24 h) at the residence of each individual was determined using noise‐dispersion models and manual noise assessments. The individual noise exposure was classified in units of 5 dB(A), from <45 dB(A) to >65 dB(A).

Results

The odds ratio (OR) for hypertension adjusted for age, smoking, occupational status and house type was 1.38 (95% confidence interval (CI) 1.06 to 1.80) per 5 dB(A) increase in noise exposure. The association seemed stronger among women (OR 1.71; 95% CI 1.17 to 2.50) and among those who had lived at the address for >10 years (OR 1.93; 95% CI 1.29 to 2.83). Analyses of categorical exposure variables suggested an exposure–response relationship. The strongest association between exposure to traffic noise and hypertension was found among those with the least expected misclassification of true individual exposure, as indicated by not having triple‐glazed windows, living in an old house and having the bedroom window facing a street (OR 2.47; 95% CI 1.38 to 4.43).

Conclusion

The results of our study suggest an association between exposure to residential road traffic noise and hypertension.Noise acts as a ubiquitous stress‐mediating factor in the physical environment. General annoyance, disturbances in psychosocial well‐being and reduction in sleep quality are commonly reported effects of noise exposure.^1,2 An increased risk of non‐auditory physiological effects due to noise, such as hypertension and ischaemic heart disease, have also been suggested.^3,4,5,6,7,8 Most previous studies have been performed in occupational settings with high noise levels.^5,6,8,9,10 Community noise is less well studied.Road traffic is the dominating source of community noise in the urban environment. Few studies have investigated an association between exposure to road traffic noise and hypertension, and the results are conflicting.^3,4,11 Studies in this field have low precision and validity problems, including crude exposure assessments, selection bias and limited control of important confounding factors. Exposure has usually been assessed either from subjective reports or without consideration of important factors that may influence the individual exposure level—for example, window type, bedroom window orientation and type of residence.The suggested biological mechanism for an association between exposure to community noise and hypertension is that noise induces stress by disturbing sleep and interfering with relaxation and concentration and many other cognitive effects that activate the sympathetic nervous system and the endocrine system.¹² The primary physiological effects of noise exposure are vegetative reactions such as increase in blood pressure, heart rate and finger pulse amplitude, cardiac arrhythmia, and changes in respiration and body movements.¹³ Therefore, a hypothesis has emerged that stress due to persistent exposure to environmental noise could result in permanent vascular changes, with increased blood pressure and ischaemic heart disease as potential outcomes.^14,15,16Our objective was to study a possible association between exposure to residential road traffic noise and hypertension among adults in an urban municipality. To better characterise individual noise exposure, we aimed at investigating factors that may influence the true exposure level, such as window type, bedroom window orientation and type of residence.     

Validity of questionnaire self-reports on computer, mouse and keyboard usage during a four-week period

Objective

To examine the validity and potential biases in self‐reports of computer, mouse and keyboard usage times, compared with objective recordings.

Methods

A study population of 1211 people was asked in a questionnaire to estimate the average time they had worked with computer, mouse and keyboard during the past four working weeks. During the same period, a software program recorded these activities objectively. The study was part of a one‐year follow‐up study from 2000–1 of musculoskeletal outcomes among Danish computer workers.

Results

Self‐reports on computer, mouse and keyboard usage times were positively associated with objectively measured activity, but the validity was low. Self‐reports explained only between a quarter and a third of the variance of objectively measured activity, and were even lower for one measure (keyboard time). Self‐reports overestimated usage times. Overestimation was large at low levels and declined with increasing levels of objectively measured activity. Mouse usage time proportion was an exception with a near 1:1 relation. Variability in objectively measured activity, arm pain, gender and age influenced self‐reports in a systematic way, but the effects were modest and sometimes in different directions.

Conclusion

Self‐reported durations of computer activities are positively associated with objective measures but they are quite inaccurate. Studies using self‐reports to establish relations between computer work times and musculoskeletal pain could be biased and lead to falsely increased or decreased risk estimates.During the last few decades personal computers have become one of the most common working tools in developed countries. In Denmark it has been estimated that by 2001 approximately 20% of the working population used a computer for at least 75% of their working time.¹ Data entry and work with visual display units in relation to musculoskeletal pain and disorders have been studied intensively, mostly in cross‐sectional studies,^2,3,4,5,6 and in recent years results from large longitudinal studies have appeared.^{7,8,9,10,11,12,13,14,15,16} Several of these studies indicate that musculoskeletal pain, especially in the distal arm regions, increases with increasing daily or weekly duration of computer work and that the increased risk of musculoskeletal pain may appear at even short daily or weekly computer work times and without any obvious threshold level. From a biological point of view, such an exposure‐response pattern seems unlikely, indicating that the relations may be biased. Different types of biases may influence the observed relations between musculoskeletal pain and computer work, including information bias with respect to self‐reports on computer work times. Almost all previous epidemiological studies have relied on self‐reported data on the duration of computer work time, yet the validity of such self‐reports has only been studied in a few smaller studies with a one‐day recording period,^17,18,19 and in one study with a recording period of 15 work days.²⁰ The present paper deals with validity and potential sources of information bias in self‐reported computer, mouse and keyboard work times during a four‐week period, based on self‐reports and objective activity data from 1211 people.     

Mortality from non-malignant respiratory diseases among people with silicosis in Hong Kong: exposure-response analyses for exposure to silica dust

Objectives

To examine the exposure–response relationships between various indices of exposure to silica dust and the mortality from non‐malignant respiratory diseases (NMRDs) or chronic obstructive pulmonary diseases (COPDs) among a cohort of workers with silicosis in Hong Kong.

Methods

The concentrations of respirable silica dust were assigned to each industry and job task according to historical industrial hygiene measurements documented previously in Hong Kong. Exposure indices included cumulative dust exposure (CDE) and mean dust concentration (MDC). Penalised smoothing spline models were used as a preliminary step to detect outliers and guide further analyses. Multiple Cox''s proportional hazard models were used to estimate the dust effects on the risk of mortality from NMRDs or COPDs after truncating the highest exposures.

Results

371 of the 853 (43.49%) deaths occurring among 2789 workers with silicosis during 1981–99 were from NMRDs, and 101 (27.22%) NMRDs were COPDs. Multiple Cox''s proportional hazard models showed that CDE (p = 0.009) and MDC (p<0.001) were significantly associated only with NMRD mortality. Subgroup analysis showed that deaths from NMRDs (p<0.01) and COPDs (p<0.05) were significantly associated with both CDE and MDC among underground caisson workers and among those ever employed in other occupations with high exposure to silica dust. No exposure–response relationship was observed for surface construction workers with low exposures. A clear upward trend for both NMRDs and COPDs mortality was found with increasing severity of radiological silicosis.

Conclusion

This study documented an exposure–response relationship between exposure to silica dust and the risk of death from NMRDs or COPDs among workers with silicosis, except for surface construction workers with low exposures. The risk of mortality from NMRDs increased significantly with the progression of International Labor Organization categories, independent of dust effects.Excessive mortality from non‐malignant respiratory diseases (NMRDs) including chronic obstructive pulmonary disease (COPD) has been reported among cohorts exposed to silica dust or among cohorts with disease silicosis.^{1,2,3,4,5,6,7} However, inconsistent or even conflicting evidence existed on the exposure–response relationship between exposure to silica dust and death from NMRDs or COPD.^{1,3,4,5,6,7,8,9} Besides the potential differences in methods or toxicity of quartz polymorphs and exposure levels, discrepancies between studies might reflect the differences in biological effectiveness of various exposure indices.^3,10 The potential limitations of cumulative dust exposure (CDE) had been emphasised by Smith,¹¹ who said that CDE might be a poor dose index in examining the association with lung diseases by using a pharmacokinetic model. Hughes et al¹² found a substantially steeper relationship with silicosis among diatomaceous earth workers exposed at the highest concentrations of crystalline silica. More recently, Buchanan et al¹³ provided supportive evidence on this issue and suggested that quantifying the risks of silicosis should take into account the variations in quartz exposure intensity, particularly for concentrations >1 or 2 mg/m³, even if exposures were for relatively short periods. Studies comparing the possible effect of cumulative exposure to silica dust and mean dust concentration (MDC) on the risk of NMRD or COPD remain sparse and in demand. We report here the exposure–response analyses between various indices of exposure to silica dust and mortality from NMRDs or COPD among a cohort of 2789 workers with silicosis in Hong Kong, taking into consideration the effect of cigarette smoking.     

Occupational risk factors for asthma among nurses and related healthcare professionals in an international study

Objective

The authors examined the relations between self‐reported work tasks, use of cleaning products and latex glove use with new‐onset asthma among nurses and other healthcare workers in the European Community Respiratory Health Survey (ECRHS II).

Methods

In a random population sample of adults from 22 European sites, 332 participants reported working in nursing and other related healthcare jobs during the nine‐year ECRHS II follow‐up period and responded to a supplemental questionnaire about their principal work settings, occupational tasks, products used at work and respiratory symptoms. Poisson regression models with robust error variances were used to compare the risk of new‐onset asthma among healthcare workers with each exposure to that of respondents who reported professional or administrative occupations during the entire follow‐up period (n = 2481).

Results

Twenty (6%) healthcare workers and 131 (5%) members of the referent population reported new‐onset asthma. Compared to the referent group, the authors observed increased risks among hospital technicians (RR 4.63; 95% CI 1.87 to 11.5) and among those using ammonia and/or bleach at work (RR 2.16; 95% CI 1.03 to 4.53).

Conclusions

In the ECRHS II cohort, hospital technicians and other healthcare workers experience increased risks of new‐onset current asthma, possibly due to specific products used at work.Nursing and other related healthcare occupations are demanding professions. Men and women in these jobs are responsible for providing high‐quality health care, but the environments in which they routinely work, including hospitals, clinics and laboratories, are increasingly recognised as hazardous workplaces.^1,2,3,4,5 In particular, inhalation exposures and their potential respiratory health effects are of growing concern among workers in healthcare settings. Findings that describe the asthmagenic and allergenic properties of specific products (eg, natural rubber latex gloves) provided the basis for efforts to reduce such exposures in many healthcare settings, but continuing exposures to cleaning agents and latex products in the workplace remain important risk factors for adult‐onset work‐related asthma.^6,7,8 Thus, further characterisation of these and other inhalation hazards in healthcare workplaces may facilitate the prevention of asthma in this important workforce.The roles and responsibilities of nurses and other healthcare workers vary widely, as do the specific occupational tasks and products used. Nonetheless, certain aspects of medical workplaces are ubiquitous. For example, alkaline glutaraldehyde, a disinfectant used to sterilise medical instruments, has been associated with respiratory symptoms among nurses,^9,10,11 hospital technicians¹¹ and respiratory therapists.¹² Recent surveillance data for cases of work‐related asthma indicate that healthcare workers are the most commonly reported industry group (16%), among which cleaning products (eg, ammonia, bleach, disinfectants and other cleaning agents) (24%), latex (20%), glutaraldehyde (9%) and formaldehyde (5%) appear as common work‐related exposures.⁶ The frequency with which latex was reported as one of the contributing exposures among workers in nursing occupations (33%) provides further evidence that latex is still a major concern for workers in healthcare settings,^6,13,14 where dermal and respiratory latex exposures have been associated with symptoms among hospital personnel.^15,16,17Data from the European Community Respiratory Health Survey (ECRHS) provide a unique opportunity to assess respiratory health effects among healthcare workers throughout Europe. Previous analysis of occupational exposures among workers in the ECRHS population suggests that occupational asthma may account for between 5% and 10% of asthma in young adults¹⁸ and that those working as nurses may experience notably increased asthma risks.¹⁹ Although a better understanding of the specific respiratory risks and exposures may lead to improvements in working conditions in this important workforce, the extent to which increased risks are attributable to specific exposures has not yet been investigated using baseline and follow‐up ECRHS data. In addition, the longitudinal ECRHS study design provides a unique opportunity to assess the role of specific healthcare‐related tasks and products in a previously symptom‐free population. Therefore, with a primary aim of assessing the potential health effects of inhalation exposures in healthcare settings, we examined the risk of new‐onset asthma among nurses and other healthcare workers who reported specific job‐related tasks, use of cleaning products and latex gloves at work.     

The recovery patterns of back pain among workers with compensated occupational back injuries

Objectives

To investigate the longitudinal patterns of recovery among workers with compensated occupational back injuries.

Methods

A longitudinal cohort study, with one‐year follow‐up via structured telephone interviews, among respondents off work because of “new” back injuries. Self‐reported pain intensity was recorded at baseline and at four follow‐up time points over the course of one year. Workers who answered the questionnaire on at least three occasions (n = 678) were classified into clusters according to their patterns of pain intensity over time using a two‐step cluster analysis.

Results

Four pain recovery patterns were identified: workers with high levels of pain intensity showing no improvement over time (43%); those experiencing recovery in the first four months with no further improvement or possibly even some deterioration, in the second half year (33%); those experiencing a slow consistent recovery but still with considerable back pain at the end of the follow‐up (12%); and those quickly progressing to low level of pain or resolution (12%). Trajectories of average Roland‐Morris Disability scores and SF‐36 Role of Physical scores for above clusters mapped consistently with the corresponding patterns in pain. However, individuals with fluctuating, recurrent pain patterns showed the shortest cumulative duration on 100% benefit and the earliest return‐to‐work among other clusters.

Conclusions

Four clinically sensible patterns were identified in this cohort of injured workers, suggesting inter‐individual differences in back pain recovery. The results confirm that recurrent or chronic back pain is a typical condition in respondents with new back injuries. Pain intensity and disability scores are good measures of recovery of back pain at the individual level. After initial return‐to‐work, or cessation of benefits, administrative measures of percentage of respondents back at work, or no longer on benefits, may not accurately reflect an individual''s condition of back pain.Low back disorders are the most common, costly and disabling of musculoskeletal health problem.¹ They are one of the most common reasons for visits to primary care,² and the single largest category of workers'' compensation claims in most compensation systems.³ While some cases of low back pain are transient and resolve or considerably improve over several weeks,^4,5 symptoms can often be recurrent or chronic.^6,7 Studies have shown that over 65% of back pain patients in primary care continued to experience at least mild pain one month after seeking care, and approximately 33% reported continuing pain of at least moderate intensity after 12 months.^5,8The course of back disorders can be characterised using measures of different aspects of health,⁹ such as pain, disability, activity limitations and/or participation.¹⁰ For instance, the course has been studied by assessing the prevalence of back pain at different time points, or by evaluating changes in the amount of pain across time in pre‐classified patient groups.^10,11,12 Transitions between different states such as resolution, improvement, aggravation and recurrence have also been used to study courses.¹³Participation in work is also a key outcome in studies of back pain. Duration of claim in workers'' compensation systems^10,14,15 and time to return to work^10,16 have also been used as end‐points in studies evaluating the duration of back‐pain episodes, or to identify prognostic factors or effective interventions. However, measures based on first return to work may underestimate the percentage of people impaired^17,18 because workers may continue to experience pain after returning to work, or may experience recurrent episodes of pain and disability. While some studies have shown a relation between pain and disability and time to claim closure,¹⁹ other factors also may influence the decision to return to work.¹⁰Von Korff described the course of back pain as highly variable, occurring in transient, recurrent, and chronic phases.⁷ Few longitudinal studies have been carried out to classify the different pathways of back pain.^13,20 Dunn et al used longitudinal latent class analysis to identify four groups of back pain patients with distinctive recovery patterns in a primary care setting.²⁰ It would be of interest to explore the course of back pain in a population of injured workers to determine similarities and differences to those among the general population.The purpose of this study is (1) to identify and summarise the course of pain in a cohort of injured workers off work because of back pain and (2) to describe the distribution of the patterns across other commonly used proxy measures of recovery.     

Association between plasma BPDE-Alb adduct concentrations and DNA damage of peripheral blood lymphocytes among coke oven workers

Objectives

Coke oven emissions (COE) containing polycyclic aromatic hydrocarbons (PAHs) can induce both benzo[a]pyrene‐r‐7, t‐8, t‐9,c‐10‐tetrahydotetrol‐albumin (BPDE‐Alb) adducts and DNA damage. However, the relation between these biomarkers for early biological effects is not well documented in coke oven workers.

Methods

In this study, the authors recruited 207 male workers exposed to COE and 102 controls not exposed to COE in the same steel plant in northern China. They measured BPDE‐Alb adduct concentrations in plasma with reverse‐phase high performance liquid chromatography and DNA damage in peripheral blood lymphocytes with alkaline comet assay.

Results

The results showed that the median concentration of BPDE‐Alb adducts in the exposed group (34.36 fmol/mg albumin) was significantly higher than that in the control group (21.90 fmol/mg albumin, p = 0.012). The mean Olive tail moment (Olive TM) of DNA damage in the exposed and control groups were 1.20 and 0.63, respectively (p = 0.000). Multivariate logistic regression analysis revealed that the odds ratio (OR) for BPDE‐Alb adduct and Olive TM associated with the exposure were 1.72 (95% CI 1.06 to 2.81) and 1.96 (95% CI 1.20 to 3.19), respectively. These results show significant correlations between the concentrations of BPDE‐Alb adduct and Olive TM levels in exposed group (r = 0.235, p = 0.001) but not in control group (r = 0.093, p = 0.353).

Conclusion

The results suggest that occupational exposure to COE may induce both BPDE–Alb adducts and DNA damage in the lymphocytes of coke oven workers and that these two markers are useful for monitoring exposure to COE in the workplace.Coke oven workers are exposed to coke oven emissions (COE) that contain a wide variety of volatile organic solvents and particulates, especially polycyclic aromatic hydrocarbons (PAHs).¹ Epidemiological studies suggest an aetiological link between carcinogenic PAHs exposure and lung cancer risk in coke oven workers exposed to COE, and coke oven workers were found to have a three‐ to sevenfold increased risk for developing lung cancer.^1,2Benzo[a]pyrene (B[a]P), the most potent and well‐studied carcinogen in PAHs mixtures, has been used as an indicator for carcinogenic PAHs.^3,4 The metabolic activation of B[a]P by cytochromes P450 produces 7,8‐dihydroxy‐9,10‐epoxy‐7,8,9,10‐tetrahydrobenzo[a]pyrene (BPDE), the ultimate carcinogenic form that can bind covalently to DNA and proteins.⁵ Therefore, both DNA and protein adducts are thought to be biologically effective dose biomarkers of PAHs.⁶ There are a number of published reports on DNA adducts in workers exposed to PAHs.^7,8 Although DNA adducts determined using DNA from white blood cells may not reflect the levels of DNA damage in the target tissues,⁹ DNA from the target tissues is usually not readily accessible in human biomonitoring. The albumin adducts in blood are considered a surrogate biomarker of the effective dose of exposure and are not considered to be directly involved in carcinogenesis,¹⁰ because they represent only one month exposure within the half‐life of the albumin.¹¹The carcinogenicity induced by PAHs compounds is believed to be initiated by DNA damage.¹² A wide variety of non‐bulky base damage and single‐strand breaks are formed during metabolic activation of PAHs and involved in PAHs carcinogenesis,^13,14 and these types of DNA damage can be detected by comet assay and used as a marker of early biological effects of DNA‐damaging agents in the living environments and occupational workplaces.^15,16,17 Specifically, the alkaline comet assay (pH>13) can detect DNA strand breaks, alkali‐labile sites, and incomplete excision repair sites.¹⁸ However, the published results of the relation between COE exposure and DNA damage in the lymphocytes measured by comet assay are not consistent.^{19,20,21,22,23} For example, some investigations have shown that there was a significant increase in DNA damage in workers exposed to COE compared with unexposed controls.^19,20,22 However, others^21,23 did not find any effect of occupational exposure on the levels of DNA damage measured with the comet assay, possibly due to small sample sizes in these studies.In the exposure‐to‐disease pathogenic pathway, biomarkers that can provide information of exposure to carcinogenic agents (biomarkers of exposure) and early changes caused by the agents (biomarkers of effect) are needed in epidemiological studies of cancer risk. However, the levels of exposure biomarkers and their associations with early biological effects in coke oven workers are not well documented. Some authors have reported significant association between biomarkers of internal dose (1‐hydroxypyrene) and effect biomarkers (comet assay, sister chromatid exchanges, micronuclei, chromosomal aberrations, and 8‐oxo‐7, 8‐dihydro‐2''‐deoxyguanosine) for coke oven workers exposed to PAHs,^20,22,23 but these were not confirmed by other studies.^21,26 One reason for this inconsistency is the levels of 1‐hydroxypyrene revealing recent exposure to COE or different sample size (from 83 to 217 subjects included). A positive association between biologically effective‐dose biomarkers (aromatic‐DNA adducts) with effect biomarkers (8‐oxo‐7, 8‐dihydro‐2''‐deoxyguanosine) among 149 coke oven workers was previously reported.²⁶ To our knowledge, there was no reported investigation on the correlation between BPDE‐Alb adduct concentrations and DNA damage in lymphocytes in coke oven workers, although these two biomarkers were individually applied in some occupational biomonitoring. Therefore, we further assessed whether occupational exposure to COE resulted in high concentrations of BPDE–Alb adducts and DNA damage and their possible correlation in 207 male workers exposed to COE and 102 male unexposed controls.     

NO2 and children's respiratory symptoms in the PATY study

Objectives

NO₂ is a major urban air pollutant. Previously reported associations between ambient NO₂ and children''s respiratory health have been inconsistent, and independent effects of correlated pollutants hard to assess. The authors examined effects of NO₂ on a spectrum of 11 respiratory symptoms, controlling for PM₁₀ and SO₂, using a large pooled dataset.

Methods

Cross sectional studies were conducted in Russia, Austria, Italy, Switzerland, and the Netherlands, during 1993–99, contributing in total 23 955 children. Study‐specific odds ratios for associations with ambient NO₂ are estimated using logistic regressions with area‐level random effects. Heterogeneity between study‐specific results, and mean estimates (allowing for heterogeneity) are calculated.

Results

Long term average NO₂ concentrations were unrelated to prevalences of bronchitis or asthma. Associations were found for sensitivity to inhaled allergens and allergy to pets, with mean odds ratios around 1.14 per 10 μg/m³ NO₂. SO₂ had little confounding effect, but an initial association between NO₂ and morning cough was reduced after controlling for PM_10. Associations with reported allergy were not reduced by adjustment for the other pollutants. Odds ratios for allergic symptoms tended to be higher for the 9–12 year old children compared with the 6–8 year old children.

Conclusions

Evidence for associations between NO₂ and respiratory symptoms was robust only for inhalation allergies. NO₂ most likely is acting as an indicator of traffic related air pollutants, though its direct effect cannot be ruled out. This remains important, as policies to reduce traffic related air pollution will not result in rapid reductions.Links between pollution and health are hardly doubted since the disastrous great London Smog and similar incidents, yet uncertainties remain about risks at lower concentrations.¹ There is also considerable debate about the pollutants responsible for observed health effects. In the recent decade much attention has been given to ambient particles, often characterised by the concentration of PM₁₀ or PM_2.5. NO₂ is one of the major gaseous air pollutants, which continues to raise concern, and it is one of the two pollutants regulated by the European Union (PM₁₀ being the other).¹ Though NO₂ is related to combustion processes in general, in outdoor urban environments, NO₂ is considered a marker for the complex of traffic related pollutants. NO₂ characterises the spatial variation of traffic related air pollution better than PM₁₀ or PM_2.5, and observed health effects of urban air pollution characterised by NO₂ have extended from impairment of lung function growth up to premature respiratory death.^2,3Most research on NO₂ and children''s health investigates acute effects. Several studies of asthmatic children found NO₂ related increases in attacks.^4,5,6,7 Some found associations with other symptoms, but no asthma exacerbation.^8,9 The large PEACE study found no consistent NO₂ effects on respiratory symptoms or lung function.¹⁰ Several studies found effects of other pollutants, but not NO₂.^11,12,13Within the literature from cross sectional studies, NO₂ is most clearly linked to cough, with consistent reports of positive (if sometimes weak) associations.^14,15,16 Slightly less evidence is found overall for an association with bronchitis, with Peters reporting a weak negative association, while others show evidence (mostly weak) of a positive association.^14,15,16,17 Estimates of associations with asthma and wheeze have been small and therefore, although varying in direction, not inconsistent with each other.^{14,15,16,17,18,19,20} Gauderman reports associations between asthma and measured NO₂, and between asthma and residence close to freeways, where traffic levels are extremely high, but no association with residence close to ordinary roads.²¹In the atmosphere, NO₂ is correlated with other pollutants including PM₁₀ and PM_2.5, because of similar sources. Pollutants'' independent effects are infrequently reported, because of their intercorrelations. Fusco found some independent NO₂ effect on acute respiratory infections.²² Braga found independent PM₁₀ effects only.²³ Some reported NO₂ effects may be due to associations with other pollutants such as ultrafine particles or diesel soot.The Pollution and the Young (PATY) project assembled health and exposure data for 58 561 children, from comparable cross sectional studies conducted in 12 countries. Pooling original data allows harmonisation of analysis, pursuit of research questions not addressed originally, and inclusion of unpublished studies. Here we examine associations between NO₂ and symptoms, in those PATY studies with NO₂ exposure data: 23 955 children aged 6–12, from five countries. We present results from single‐ and multipollutant models, exploiting the opportunity this pooled study gives to attempt to assess effects of NO₂, adjusted for other major pollutants (SO₂ and PM10). We further make use of the large dataset to assess effect modification with more precision than single studies.     

Respiratory health and individual estimated exposure to traffic-related air pollutants in a cohort of young children

Objectives

To estimate long‐term exposure to traffic‐related air pollutants on an individual basis and to assess adverse health effects using a combination of air pollution measurement data, data from geographical information systems (GIS) and questionnaire data.

Methods

40 measurement sites in the city of Munich, Germany were selected at which to collect particulate matter with a 50% cut‐off aerodynamic diameter of 2.5 µm (PM_2.5) and to measure PM_2.5 absorbance and nitrogen dioxide (NO₂). A pool of GIS variables (information about street length, household and population density and land use) was collected for the Munich metropolitan area and was used in multiple linear regression models to predict traffic‐related air pollutants. These models were also applied to the birth addresses of two birth cohorts (German Infant Nutritional Intervention Study (GINI) and Influence of Life‐style factors on the development of the Immune System and Allergies in East and West Germany (LISA)) in the Munich metropolitan area. Associations between air pollution concentrations at birth address and 1‐year and 2‐year incidences of respiratory symptoms were analysed.

Results

The following means for the estimated exposures to PM_2.5, PM_2.5 absorbance and NO₂ were obtained: 12.8 μg/m³, 1.7×10⁻⁵ m⁻¹ and 35.3 μg/m³, respectively. Adjusted odds ratios (ORs) for wheezing, cough without infection, dry cough at night, bronchial asthma, bronchitis and respiratory infections indicated positive associations with traffic‐related air pollutants. After controlling for individual confounders, significant associations were found between the pollutant PM_2.5 and sneezing, runny/stuffed nose during the first year of life (OR 1.16, 95% confidence interval 1.01 to 1.34) Similar effects were observed for the second year of life. These findings are similar to those from our previous analysis that were restricted to a subcohort in Munich city. The extended study also showed significant effects for sneezing, running/stuffed nose. Additionally, significant associations were found between NO₂ and dry cough at night (or bronchitis) during the first year of life. The variable “living close to major roads” (<50 m), which was not analysed for the previous inner city cohort with birth addresses in the city of Munich, turned out to increase the risk of wheezing and asthmatic/spastic/obstructive bronchitis.

Conclusions

Effects on asthma and hay fever are subject to confirmation at older ages, when these outcomes can be more validly assessed.Only a few studies, mainly in Europe, have investigated the effects of traffic‐related air pollution on human health. There is an ongoing debate about long‐term exposure to traffic‐related air pollutants, as chronic effects on respiratory health^1,2,3 and even mortality have been documented in several studies.^4,5 With respect to health effects, the most common investigated traffic‐related air pollutant is particulate matter.As a major source of particulate matter, traffic substantially contributes to the overall effect of outdoor air pollution.⁶ Although epidemiological research is needed, exposure assessment issues for traffic‐related air pollutants are complex and need to be considered before undertaking investigations of health effects. As vehicle emissions, by definition, take place on roads, people who live close to major roads might be expected to be exposed to higher concentrations of traffic‐related air pollutants and have a higher risk of adverse health effects. Several studies have shown higher rates of respiratory illness and symptoms and reduced lung functions in people living close to busy roads.^{1,7,8,9,10,11,12,13} Several studies showed that exposure to nitrogen dioxide (NO₂)^14,15 and particulate matter,¹⁶ as well as proximity to motorways,¹⁷ are associated with respiratory health symptoms.A powerful tool to estimate individual exposure to traffic‐related air pollutants is geographical information systems (GIS)‐based modelling. GIS provides the means to capture, store, process and display spatial data. In contrast with self‐reported traffic intensities, GIS models have a lot of advantages.^18,19 Assessments of exposure to traffic‐related air pollutants based on questionnaire reports, for example, can lead to serious misclassifications. Thus, individuals may overestimate the traffic intensity in their neighbourhood as high, even if the traffic load in the whole community is low.GIS‐based models can also include information from larger areas by taking different buffer zones into account. Up to now, only a few studies have combined geographical data with concentration measurements to calculate individual exposure.^2,20,21,22In the framework of the European Union‐funded Traffic‐Related Air Pollution and Childhood Asthma (TRAPCA) project, regression models were developed and applied to the residential addresses of 1756 children who lived in the city of Munich, Germany.² We extended our existing model²³ to the Munich metropolitan area, which includes the city of Munich and surrounding districts. Using the extended study population of this area, we tested the hypothesis whether increased exposure to traffic‐related air pollutants in children is associated with a higher risk of developing inhalant allergy, asthma or other chronic respiratory conditions than in children with low exposure.For this study, we developed GIS‐based regression models for particulate matter with a 50% cut‐off aerodynamic diameter of 2.5 µm (PM_2.5), PM_2.5 absorbance and NO₂ for the Munich metropolitan area and applied these models to the residential addresses of the members of two birth cohorts. Further, we analysed the association between exposure to traffic‐related air pollutants, living close to major roads and health effects at 2 years of life.