Allergy and cancer: organ site-specific results from the Adventist Health Study.

The relation between allergy and risk of cancer was evaluated in a cohort study of 34,198 Seventh-day Adventists in California. Information on prevalence of asthma, hay fever, and reactions to chemicals, medications, bee stings, and poison oak (or ivy) was obtained by questionnaire in 1976. The reported allergies must have been serious enough to require treatment by a physician. The cohort was then followed for 6 years (1977-1982). Both stratified analysis and Cox proportional hazards regression analyses were utilized to evaluate the relation of allergy to cancer after taking into account several potentially confounding variables. For all cancer sites combined in males, there was a 33% increased risk associated with reaction to medications. In contrast, among females, reaction to medications was associated with a 21% decrease in risk. Both results were statistically significant. Prostate and breast cancer risk were elevated in persons who reported any type of allergic history, as was risk of lymphatic or hematopoietic cancers and sarcoma. For each of these types of cancer, risk increased with increasing numbers of allergies. However, ovarian cancer risk was decreased in persons with any allergic history and increasing numbers of allergies was associated with decreasing risk of this form of cancer. These results suggest that the association between allergy and cancer is complex and depends on the specific allergy and the specific organ site under consideration.     

Bladder cancer in a low risk population: results from the Adventist Health Study

A cohort study of bladder cancer was conducted in a population of California Seventh-day Adventists. Most Seventh-day Adventists use neither tobacco nor alcohol yet experience a large degree of variation in dietary habits. Therefore, diet and other lifestyle habits were evaluated in this unique population. In 1976, 34,198 non-Hispanic white Seventh-day Adventists in California completed a detailed lifestyle questionnaire which included a 51-item food frequency section. This cohort was then followed until the end of 1982 during which time all newly diagnosed malignancies were detected. In order to evaluate the relation between several variables hypothesized to be associated with altered bladder cancer risk, age-, sex-, and smoking-adjusted relative risks (incidence rate ratios) were calculated using the method of Mantel-Haenszel adopted for person-time data. Multivariate analyses were conducted using the Cox Proportional Hazards Regression model. Between the return of the questionnaire and the end of follow-up, there were 52 histologically confirmed bladder cancers detected in the cohort. Increasing age, male gender, and a history of cigarette smoking were all significantly associated with increased bladder cancer risk. In addition, residence in a rural area was associated with significantly increased risk (relative risk (RR) = 1.80) as was high consumption of meat, poultry, and fish (RR = 2.57).     

Evaluation of the agreement between modeled and monitored ambient hazardous air pollutants in California

Elevated breast cancer incidence rates in urban areas have led to speculation regarding the potential role of air pollution. In order to inform the exposure assessment for a subsequent breast cancer study, we evaluated agreement between modeled and monitored hazardous air pollutants (HAPs). Modeled annual ambient concentrations of HAPs in California came from the US Environmental Protection Agency’s National Air Toxics Assessment database for 1996, 1999, 2002, and 2005 and corresponding monitored data from the California Air Resources Board’s air quality monitoring program. We selected 12 compounds of interest for our study and focused on evaluating agreement between modeled and monitored data, and of temporal trends. Modeled data generally underestimated the monitored data, especially in 1996. For most compounds agreement between modeled and monitored concentrations improved over time. We concluded that 2002 and 2005 modeled data agree best with monitored data and are the most appropriate years for direct use in our subsequent epidemiologic analysis.     

Effects of ambient air pollutants on asthma medication use and wheezing among fourth-grade school children from 12 Southern California communities enrolled in The Children's Health Study

To investigate the effects of 12 monthly average air pollution levels on monthly prevalence of respiratory morbidity, the authors examined retrospective questionnaire data on 2034 4th-grade children from 12 Southern California communities that were enrolled in The Children's Health Study. Wheezing during the spring and summer months was associated with community levels of airborne particulate matter with a diameter < or = 10 microm (PM10) (odds ratio (OR) = 2.91; 95% confidence interval (CI) = 1.46-5.80), but was not associated with community levels of ozone, nitrogen dioxide, PM2.5 (diameter < or = 2.5), nitric acid, or formic acid. Logistic regression was performed on data stratified into two seasonal groups, spring/summer and fall/winter. Among asthmatics, the monthly prevalence of asthma medication use was associated with monthly levels of ozone, nitric acid, and acetic acid (OR = 1.80 [95%CI = 1.19-2.70]; OR = 1.80 [95%CI = 1.23-2.65]; OR = 1.57 [95% CI = 1.11-2.21]; respectively). Asthma medication use was more prevalent among children who spent more time outdoors--with consequential exposure to ozone--than among children who spent more time indoors (OR = 3.07 [95%CI = 1.61-5.86]; OR = 1.31 [95%CI = 0.47-2.71]; respectively). The authors concluded that monthly variations in some ambient air pollutants were associated with monthly respiratory morbidity among school children.     

Long-term effects of ambient air pollution on lung function: a review

Lung function is an important measure of respiratory health and a predictor of cardiorespiratory morbidity and mortality. Over the past 2 decades, more than 50 publications have investigated long-term effects of ambient air pollution on lung function with most finding adverse effects. Several studies have also suggested effects from traffic-related air pollution. There is strong support for air pollution effects on the development of lung function in children and adolescents. It remains unclear whether subjects with slower development of lung function compensate by prolonging the growth phase, or whether they end their development at a lower plateau, thus entering the decline phase with a reduced lung function. In adults, the evidence for long-term air pollution effects is mostly based on cross-sectional comparisons. One recent longitudinal study observed that decreasing pollution attenuated the decline of lung function in adults. Earlier inconclusive cohort studies were based on limited data. There is great diversity in study designs, markers of air pollution, approaches to the measurement of exposure, and choices in lung function measures. These limit the comparability of studies and impede quantitative summaries. New studies should use individual-level exposure assessment to clarify the role of traffic and to preclude potential community-level confounding. Further research is needed on the relevance of specific pollution sources, particularly with regard to susceptible populations and relevant exposure periods throughout life.     

Estimating cumulative ambient concentrations of air pollutants: description and precision of methods used for an epidemiological study

Methods for estimating cumulative ambient air pollution concentrations for individuals enrolled in an epidemiological cohort study are described and studied. Monthly interpolations from fixed-site monitoring stations in California to zip code centroids were used. The precision of the interpolation methods for total suspended particulates and ozone was assessed, and fixed-site monitoring stations were used in turn as receptor sites. Actual versus interpolated 2-y mean concentrations did not differ significantly and were correlated with a Pearson correlation coefficient of .78 for total suspended particulates and .87 for ozone. The impact of the change from monitoring total oxidants to ozone on oxidant/ozone cumulations was evaluated, and monthly mean concentrations for total oxidants were compared with ozone for 435 station months during which both pollutants were measured simultaneously. Average concentrations did not differ significantly and were highly correlated (r = 0.94). Exceedance frequency statistics, which averaged slightly higher for ozone than for total oxidants, were also highly correlated.     

Estimating cancer risk from outdoor concentrations of hazardous air pollutants in 1990

A public health concern regarding hazardous air pollutants (HAPs) is their potential to cause cancer. It has been difficult to assess potential cancer risks from HAPs, due primarily to lack of ambient concentration data for the general population. The Environmental Protection Agency's Cumulative Exposure Project modeled 1990 outdoor concentrations of HAPs across the United States, which were combined with inhalation unit risk estimates to estimate the potential increase in excess cancer risk for individual carcinogenic HAPs. These were summed to provide an estimate of cancer risk from multiple HAPs. The analysis estimates a median excess cancer risk of 18 lifetime cancer cases per 100,000 people for all HAP concentrations. About 75% of estimated cancer risk was attributable to exposure to polycyclic organic matter, 1,3-butadiene, formaldehyde, benzene, and chromium. Consideration of some specific uncertainties, including underestimation of ambient concentrations, combining upper 95% confidence bound potency estimates, and changes to potency estimates, found that cancer risk may be underestimated by 15% or overestimated by 40-50%. Other unanalyzed uncertainties could make these under- or overestimates larger. This analysis used 1990 estimates of concentrations and can be used to track progress toward reducing cancer risk to the general population.     

Childhood cancer incidence rates and hazardous air pollutants in California: an exploratory analysis

Hazardous air pollutants (HAPs) are compounds shown to cause cancer or other adverse health effects. We analyzed population-based childhood cancer incidence rates in California (USA) from 1988 to 1994, by HAP exposure scores, for all California census tracts. For each census tract, we calculated exposure scores by combining cancer potency factors with outdoor HAP concentrations modeled by the U.S. Environmental Protection Agency. We evaluated the relationship between childhood cancer rates and exposure scores for 25 potentially carcinogenic HAPs emitted from mobile, area, and point sources and from all sources combined. Our study period saw 7,143 newly diagnosed cancer cases in California; of these, 6,989 (97.8%) could be assigned to census tracts and included in our analysis. Using Poisson regression, we estimated rate ratios (RRs) adjusted for age, race/ethnicity, and sex. We found little evidence for elevated cancer RRs for all sites or for gliomas among children living in high-ranking combined-source exposure areas. We found elevated RRs and a significant trend with increasing exposure level for childhood leukemia in tracts ranked highest for exposure to the combined group of 25 HAPs (RR = 1.21; 95% confidence interval, 1.03, 1.42) and in tracts ranked highest for point-source HAP exposure (RR = 1.32; 95% confidence interval, 1.11, 1.57). Our findings suggest an association between increased childhood leukemia rates and high HAP exposure, but studies involving more comprehensive exposure assessment and individual-level exposure data will be important for elucidating this relationship.     

Disability and preventive cancer screening: results from the 2001 California Health Interview Survey

OBJECTIVE: We sought to evaluate preventive cancer screening compliance among adults with disability in California. METHODS: We used data from the 2001 California Health Interview Survey to compare disabled and nondisabled adults for differences in preventive cancer screening behaviors. Compliance rates for cancer screening tests (mammography, Papanicolaou test, prostate-specific antigen, sigmoidoscopy/colonoscopy, and fecal occult blood test) between the 2 subpopulations were evaluated. RESULTS: Women with disabilities were 17% (Papanicolaou tests) and 13% (mammograms) more likely than women without disabilities to report noncompliance with cancer screening guidelines. Interactions between disability and reports of a doctor recommendation on cervical cancer screening were significant; women with disabilities had a lower likelihood of receiving a recommendation. Men with disabilities were 19% less likely than men without disabilities to report a prostate-specific antigen test within the last 3 years. CONCLUSIONS: secondary to structural and/or clinical factors underpinning the differences found.     

The adverse effect of low levels of ambient air pollutants on lung function growth in preadolescent children.

The main purpose of our study was to assess the effect of low concentrations of ambient air pollution on lung function growth in preadolescent children. We accounted for height velocity over the follow-up period and also for other possible confounders such as baseline anthropometric and physiologic characteristics of children. In addition to outdoor air pollution, we considered the possible effects of social class and exposure to indoor pollutants such as gas stove fumes or environmental tobacco smoke. The cohort prospective study was carried out in 1,001 preadolescent children from two areas of Krakow, Poland, that differed in ambient air pollutants. In the city center (higher pollution area), the mean annual level [+/- standard deviation (SD)] of suspended particulate matter was 52.6 +/- 53.98 microg/m(3) and that of SO(2) was 43.87 +/- 32.69 microg/m(3); the corresponding values in the control area were 33.23 +/- 35.99 microg/m(3) and 31.77 +/- 21.93 microg/m(3). Mean lung function growth rate adjusted to height velocity and lung function level at the study entry was significantly lower in boys and girls living in the more polluted areas. Also, the proportion of children with the slower lung function growth (SLFG) was higher in the children from the more polluted area of the city. The analysis completed in the group of children after the exclusion of asthmatic subjects and those with asthmalike symptoms confirmed that, in boys, odds ratios (ORs) for SLFG [forced vital capacity (FVC)] and air pollution after adjustment to baseline FVC, height, and growth rate was significant [OR = 2.15; 95% confidence interval (CI), 1.25-3. 69)]. The analysis also confirmed that for SLFG(FEV(1)) the OR was 1. 90 (CI, 1.12-3.25). The corresponding OR values in girls were insignificant (OR = 1.50; CI, 0.84-2.68 and OR = 1.39; CI, 0.78-2. 44). The association between ambient pollutants and poorer gain of pulmonary volumes in children living in more polluted areas suggests that air pollution in the residence area may be a part of the causal chain of reactions leading to retardation in pulmonary function growth during the preadolescent years.     

Effect of occupational air pollutants on various histological types of lung cancer: a population based case-control study.

A population based case-control study was performed in Cracow, Poland, to determine the effect of occupational air pollutants on various histological types of lung cancer. Male cases and controls were identified from the Cracow Death Register. Information was obtained by mailed questionnaire from next of kin on smoking, occupational branch, occupational exposures, and other pertinent variables. Response rates were 73.5% in cases and 72.0% in controls. For cases that underwent a bronchial biopsy or surgical excision the histological diagnosis of the tumour was obtained from clinical records. The case group contained 343 subjects with squamous cell carcinomas, 151 with small cell carcinomas, and 106 with adenocarcinomas. Twenty seven cases showed other histological types (large cell carcinoma and not classifiable). Analysis was performed separately by histological type for occupational exposure variables adjusted for smoking. Long term exposure to mineral dust and metal dust (20 years or more) was found to be a significant risk factor for small cell and squamous cell carcinoma. The effect was more pronounced if the analysis was restricted to those aged less than 70 years. The highest relative risk (RR) due to occupational exposures was found for squamous cell carcinoma and exposure to mineral dust for more than 20 years (RR = 2.45, 95% CI 1.43-4.19). The estimated effect of mineral dust on small cell carcinoma and adenocarcinoma was smaller (RR = 2.29, 95% CI 1.16-4.53 and RR = 2.04, 95% CI 0.89-4.64 respectively). The effect of metal dust and fumes seemed about the same for squamous and small cell carcinoma. No specific agent could be identified as particularly important for a specific histological type; it rather seemed that the effects of the substances considered were similar for lung cancers in general.     

大气污染物致肺癌的潜伏期灰色定量分析

目的：测算大气污染物致肺癌的潜伏期。方法：利用灰色系统理论中的灰色关联度模型，根据最大关联度值测算出总体的潜伏期。结果：总悬浮颗粒物（TSP）的最大关联度值为0.886，所对应的是1985－1989年的比较数列与1994－1998年的参考数列的关系最为密切。二氧化硫（SO2）的最大关联度值为0.919，的是1986－1990年的比较数列与1994－1998年的参考数列的关系最为密切。结论：H市SO2和TSP致肺癌的潜伏期分别为7年和8年。该方法不受混杂因素的制约，且计算较为简便，为大气污染物致肺癌的潜伏期研究提供一种可行和实用的新途径。     

Biomarkers of ambient air pollution and lung cancer: a systematic review

The association between ambient air pollution exposure and lung cancer risk has been investigated in prospective studies and the results are generally consistent, indicating that long-term exposure to air pollution may cause lung cancer. Despite the prospective nature and consistent findings of these studies, causality assessment can benefit from biomarker research. In the present systematic review, we assess the contribution of intermediate biomarkers in epidemiological studies, to ascertain whether their measurement reinforces causal reasoning. We have reviewed 524 papers which described the relationships between ambient air pollution and biological markers of dose and early response. The evidence for each marker was evaluated using assessment criteria which rate a group of studies from A (strong) to C (weak) on amount of evidence, replication of findings, and protection from bias. Biomarkers that scored A or B for all three criteria are included here. The markers that fulfilled the inclusion criteria are: 1-hydroxypyrene, DNA adducts, chromosomal aberrations, micronuclei, oxidative damage to nucleobases, and methylation changes. These biomarkers cover the whole spectrum of disease onset and progression from external exposure to tumour formation and some have also been suggested as risk predictors of future cancer, reinforcing causal reasoning. However, methodological issues such as confounding, publication bias and use of surrogate tissues instead of target tissues in studies on these markers are of concern. The identified biological markers have potential to shed light on the pathways of carcinogenesis, thus defining the association more clearly for public health interventions.     

Cell type specificity of female lung cancer associated with sulfur dioxide from air pollutants in Taiwan: An ecological study

Background  

Many studies have examined the association between air pollutants (including sulfur dioxide [SO₂], carbon monoxide [CO], nitrogen dioxide [NO₂], nitric oxide [NO], ozone [O₃], and particulate matter < 10 μm [PM₁₀]) and lung cancer. However, data from previous studies on pathological cell types were limited, especially for SO₂ exposure. We aimed to explore the association between SO₂ exposure from outdoor air pollutants and female lung cancer incidence by cell type specificity.     

Vanadium in ambient air: concentrations in lung tissue from autopsies of Mexico City residents in the 1960s and 1990s

Vanadium concentrations in lung tissue were determined by atomic absorption spectrometry from autopsy specimens taken from residents of Mexico City during the 1960s and 1990s (20 males and 19 females, and 30 males and 18 females, respectively). Samples from the 1990s had significantly increased mean vanadium concentrations (mean +/- standard deviation: 1.36 +/- 0.08), compared with those from the 1960s (1.04 +/- 0.05). Concentrations were not correlated with gender, smoking habit, age, cause of death, or occupation. These findings suggest that vanadium in ambient air is increasing and it represents a potential health hazard for Mexico City residents. Air pollution monitoring efforts should include vanadium concentrations in suspended particles to follow-up the findings reported herein. Researchers need to acquire a better knowledge of the levels of airborne vanadium exposure at which risk to human health occurs.     

Whole grain intake and incident endometrial cancer: the Iowa Women's Health Study.

We examined whether there is an association between whole grain intake and incident endometrial cancer and whether the association varied by use of hormone replacement therapy. The study included 23,014 Iowa women, aged 55-69 years in 1986. A mailed food frequency questionnaire was used to estimate grain intake, hormone replacement therapy use, and other cancer risk factors. Cancer incidence from 1986 to 1998 was also collected. In analyses stratified by hormone replacement therapy use, an inverse association between whole grain intake and endometrial cancer was observed among never-users of hormone replacement therapy (p for trend = 0.05). Never-users in the highest quintile of whole grain intake were 0.63 times as likely to develop endometrial cancer as those in the lowest quintile of whole grain intake (95% confidence interval = 0.39-1.01). Among hormone replacement therapy users, no association between whole grain intake and endometrial cancer was evident. There was no statistically significant association between whole grain intake and incident endometrial cancer when users of hormone replacement therapy and nonusers were analyzed together. There also was no association between refined grain intake and endometrial cancer. Whole grain intake may protect against endometrial cancer among never-users of hormone replacement therapy.     

Association of incident lung cancer with family history of female reproductive cancers: the Iowa Women's Health Study

A number of studies have documented the familial aggregation of lung cancer; there is at least one report that female reproductive cancers are also increased in these families. To determine if the risk exists for all reproductive cancer sites, we conducted a nested case-control study of lung cancer incidence in a cohort of 41,837 women ages 55-69 years. Women were recruited by mail and asked to provide information on education, occupation, smoking habits, physical activity, and family history of specific cancer sites among female relatives. Four year follow-up for cancer incidence was conducted using a state-wide tumor registry. Compared to random controls (n = 1900), cases (n = 152) were more likely to have reported at baseline a sister affected with cancer of the uterus [crude odds ratio (OR) = 3.4, 95% Cl = 1.7-7.0, P less than 0.01], cervix (OR = 3.2, 95% Cl 1.2-8.6, P less than 0.05), or cancer at any site (OR = 1.6, 95% Cl 1.1-2.4, P less than 0.05). A family history of an affected mother with a female reproductive cancer was also more common among the cases, but not statistically significant. Cases were less educated, more likely to work in a technical/industrial setting, less physically active, more likely to smoke, and to smoke for a longer period of time than the controls (all P less than 0.01). These differences reduced the magnitude of the family history risk indicators; only the combined category of reproductive cancer at all sites among sisters remained statistically significant. Additional family studies should be done to assess environmental factors in the relatives of the cases and controls to disentangle the influence of shared genes and shared environmental factors in these associations.     

Modification of the association between ambient air pollution and lung function by frailty status among older adults in the cardiovascular health study

The susceptibility of older adults to the health effects of air pollution is well-recognized. Advanced age may act as a partial surrogate for conditions associated with aging. The authors investigated whether gerontologic frailty (a clinical health status metric) modified the association between ambient level of ozone or particulate matter with an aerodynamic diameter less than 10 μm and lung function in 3,382 older adults using 7 years of follow-up data (1990-1997) from the Cardiovascular Health Study and its Environmental Factors Ancillary Study. Monthly average pollution and annual frailty assessments were related to up to 3 repeated measurements of lung function using cumulative summaries of pollution and frailty histories that accounted for duration as well as concentration. Frailty history was found to modify long-term associations of pollutants with forced vital capacity. For example, the decrease in forced vital capacity associated with a 70-ppb/month greater cumulative sum of monthly average ozone exposure was 12.3 mL (95% confidence interval: 10.4, 14.2) for a woman who had spent the prior 7 years prefrail or frail as compared with 4.7 mL (95% confidence interval: 3.8, 5.6) for a similar woman who was robust during all 7 years (interaction P < 0.001).     

Correlation between the arsenic concentrations in the air and the SMR of lung cancer

Objectives  To verify whether the concentrations of arsenic (As) and its compounds in the air (referred to here as arsenic concentrations) affect the standardized mortality ratio (SMR) associated with lung cancer. Methods  Using monitoring survey data on arsenic concentrations published by the Ministry of the Environment, we classified the municipalities for which arsenic concentrations were measured (measured municipalities) into ten groups according to the average arsenic concentration. We then determined the SMR of lung cancer, stomach cancer, pneumonia, cerebrovascular disease and cardiac disease for each group using socio-demographic data, such as the national census and demographic trends. The relationships between these factors were compared and investigated by statistical means. Results  No effect of arsenic concentrations on stomach cancer, cerebrovascular disease or cardiac disease was observed, and while significant differences in pneumonia were observed among several of the male subjects, there were no significant effects of arsenic concentration. However, lung cancer and arsenic concentration showed a significantly positive correlation for both males and females (males: Spearman r = 0.709, P < 0.05; females: Spearman r = 0.758, P < 0.05). The probability of type α error was less than 5% in areas with more than 1.77 ng As/m³ (71st percentile) and less than 1% in areas with more than 2.70 ng As/m³ (91st percentile). These results confirm that the SMR of lung cancer tends to be higher than the national average in areas of higher arsenic concentrations. Conclusions  The SMR of lung cancer is significantly higher in areas with arsenic concentrations of 1.77 ng/m³ or more.     

Fine particulate air pollution and mortality in nine California counties: results from CALFINE

Many epidemiologic studies provide evidence of an association between daily counts of mortality and ambient particulate matter<10 microm in diameter (PM10). Relatively few studies, however, have investigated the relationship of mortality with fine particles [PM<2.5 microm in diameter (PM2.5)], especially in a multicity setting. We examined associations between PM2.5 and daily mortality in nine heavily populated California counties using data from 1999 through 2002. We considered daily counts of all-cause mortality and several cause-specific subcategories (respiratory, cardiovascular, ischemic heart disease, and diabetes). We also examined these associations among several subpopulations, including the elderly (>65 years of age), males, females, non-high school graduates, whites, and Hispanics. We used Poisson multiple regression models incorporating natural or penalized splines to control for covariates that could affect daily counts of mortality, including time, seasonality, temperature, humidity, and day of the week. We used meta-analyses using random-effects models to pool the observations in all nine counties. The analysis revealed associations of PM2.5 levels with several mortality categories. Specifically, a 10-microg/m3 change in 2-day average PM2.5 concentration corresponded to a 0.6% (95% confidence interval, 0.2-1.0%) increase in all-cause mortality, with similar or greater effect estimates for several other subpopulations and mortality subcategories, including respiratory disease, cardiovascular disease, diabetes, age>65 years, females, deaths out of the hospital, and non-high school graduates. Results were generally insensitive to model specification and the type of spline model used. This analysis adds to the growing body of evidence linking PM2.5 with daily mortality.