Maternal occupational exposure during pregnancy and the risk of spina bifida.

OBJECTIVES: A case-control study was carried out to explore associations between spina bifida and occupational exposure of the mother. METHODS: The cases were children with spina bifida aperta born between 1980 and 1992 from nine hospitals in the Netherlands. The controls were children born healthy in the same period as the cases, from hospitals and from the general population. Data collection was carried out in two steps. Firstly, postal questionnaires were sent to all the parents of cases and controls to gather information on occupations and potential confounders. In the second phase of the study, information on specific exposures was collected by means of job and task specific personal interviews. Interviews were performed with 55 case mothers and 66 control mothers who had occupations with a potential for chemical or physical exposure. Those exposures were assumed to be negligible for--for example, teachers and secretaries, so personal interviews were not indicated for these women. Information was collected on specific tasks in the period just after conception, and on the associated use of chemical or physical agents, frequency of exposure, and use of protective equipment. RESULTS: The analyses of occupation showed an increased risk for women working in agricultural occupations (OR = 3.4, CI:1.3-9.0), and, although less distinct, for cleaning women (OR = 1.7, CI:0.9-3.4). Only a few women seemed to be occupationally exposed to chemical or physical agents. No differences in occurrence of specific exposures could be detected between cases and controls. Besides, no differences were seen in pesticide or disinfectant exposure among case and control mothers in agricultural occupations. CONCLUSIONS: Occupational exposures of the mother during pregnancy were infrequent and did not seem to play an important part in the aetiology of spina bifida in this study. The association found between spina bifida and maternal agricultural occupations could not be explained by the use of pesticides by the mother or by any other occupational exposure.     

Maternal and paternal occupational exposure to agricultural work and the risk of anencephaly

Aims

To evaluate the association between parental occupational exposure to agricultural work and the risk of anencephaly in three Mexican states.

Methods

A paired case control study (1:1) was done based on records of the Epidemiological Surveillance System of Neural Tube Defects in Mexico; 151 cases of anencephaly of more than 20 weeks'' gestation were selected between March 2000 and February 2001. Controls were selected from the same maternity services as those of the cases and were born alive without congenital malformations. Information was obtained from both parents by means of a general questionnaire, a food frequency questionnaire, and a specific questionnaire on occupational exposure to pesticides. Exposures were analysed with emphasis on the three months before and one month after the last menstruation periods (acute risk period (ARP)), as well as exposure prior to the abovementioned period (non‐acute risk period (NARP)).

Results

The children of mothers who worked in agriculture in the ARP had a greater risk of anencephaly (OR = 4.57, 95% CI 1.05 to 19.96). The risk of fathers having a child with anencephaly was greater in those who applied pesticides irrespective of whether it was done in the ARP or the NARP (OR = 2.50, 95% CI 0.73 to 8.64; and OR = 2.03, 95% CI 0.58 to 7.08, respectively).

Conclusions

These results support the hypothesis of the effect of maternal exposure to agricultural work on anencephaly and suggest that exposure of the father to pesticides in the periconceptional period or prior to this can also increase the risk of having an anencephalic child.     

Maternal occupational exposure and risk of specific birth defects

BACKGROUND: Gregg identified the teratogenic effect of maternal rubella infection in 1941 and since then there has been a focus on risk factors for birth defects. In nearly 70% of all birth defects, there is still no known risk factor and close to 30% of all pregnancies end in a foetal loss or spontaneous abortion, often because of a defect in the foetus. A large percentage of the workforce consists of women of reproductive age. METHODS: A search in MEDLINE for original literature and examination of the association between exposure during pregnancy and the risk of birth defects. RESULTS: Five specific birth defects were identified: neural tube defects, cleft lip and cleft palate, congenital heart defects, urinary tract defects and limb defects. The next step was to include studies with information on occupational exposure during pregnancy. CONCLUSION: There seems to be growing concern as to whether organic solvents, including glycol ethers, pesticides and heavy metals may play a teratogenic role. There is no convincing evidence linking occupational exposure during pregnancy and birth defects.     

Maternal occupational exposure and congenital malformations.

A case-referent study was conducted to assess the risk of congenital malformations in relation to maternal occupational exposure before and during pregnancy. Three hundred and twenty-five cases of major malformations and 325 normal (at birth) referents identified in 15 maternity hospitals were included in the study. The occupational history obtained from an interview of the mother was blindly reviewed by an industrial hygienist who assessed the presence of chemical exposure and the probability of exposure. The results suggested that mothers of the case children with oral clefts were more often exposed to solvents during pregnancy [odds ratio (OR) 7.9, 90% confidence interval (90% CI) 1.8-44.9] and worked more often as cleaners (four cases, no referents). Digestive anomalies (OR 11.9, 90% CI 2.0-149) and multiple anomalies (OR 4.5, 90% CI 1.4-16.9) were also associated with occupational exposure to solvents at work. These results were not modified when differences in maternal age, area of residence, and socioeconomic status were taken into account.     

Maternal exposure to occupational solvents and childhood leukemia

Many organic solvents are considered probable carcinogens. We carried out a population-based case-control study including 790 incident cases of childhood acute lymphoblastic leukemia and as many healthy controls, matched on age and sex. Maternal occupational exposure to solvents before and during pregnancy was estimated using the expert method, which involves chemists coding each individual's job for specific contaminants. Home exposure to solvents was also evaluated. The frequency of exposure to specific agents or mixtures was generally low. Results were generally similar for the period ranging from 2 years before pregnancy up to birth and for the pregnancy period alone. For the former period, the odds ratio (OR), adjusted for maternal age and sex, for any exposure to all solvents together was 1.11 [95% confidence interval (CI), 0.88-1.40]. Increased risks were observed for specific exposures, such as to 1,1,1-trichloroethane (OR = 7.55; 95% CI, 0.92-61.97), toluene (OR = 1.88; 95% CI, 1.01-3.47), and mineral spirits (OR = 1.82; 95% CI, 1.05-3.14). There were stronger indications of moderately increased risks associated with exposure to alkanes (C5-C17; OR = 1.78; 95% CI, 1.11-2.86) and mononuclear aromatic hydrocarbons (OR = 1.64; 95% CI, 1.12-2.41). Risk did not increase with increasing exposure, except for alkanes, where a significant trend (p = 0.04) was observed. Home exposure was not associated with increased risk. Using an elaborate exposure coding method, this study shows that maternal exposure to solvents in the workplace does not seem to play a major role in childhood leukemia.     

Effect of parents' occupational exposures on risk of stillbirth, preterm delivery, and small-for-gestational-age infants

Epidemiologic research on the effects of parental occupational exposures on fetal development has been limited. The National Natality and Fetal Mortality surveys obtained applicable data on probability samples of live births and fetal deaths which occurred in the US in 1980 among married women. Analyses were conducted for case groups of stillbirths (2,096 mothers, 3,170 fathers), preterm deliveries (less than 37 weeks completed gestation) (363 mothers, 552 fathers), and small-for-gestational-age infants (218 mothers, 371 fathers) compared with controls. Occupational exposures were defined by industry of employment and by imputed exposures based on a job-exposure linkage system. For stillbirth, maternal work in the rubber, plastics, and synthetics industry (odds ratio (OR) = 1.8, 95% confidence interval (Cl) 0.8-4.0) and lead exposure (OR = 1.6, 95% Cl 0.8-3.1), and paternal employment in the textile industry (OR = 1.9, 95% Cl 1.2-2.9), had the largest odds ratios. Preterm birth was most strongly associated with maternal lead exposure (OR = 2.3, 95% Cl 0.7-7.0), corroborating previous findings. Twofold increased risk of preterm delivery was found with paternal employment in the glass, clay, and stone; textile; and mining industries. Paternal exposures to x-rays and polyvinyl alcohol were associated with 1.5-fold increase in risk. The occupation of the mother was not associated with delivery of a small-for-gestational-age infant, in contrast to paternal employment in the art (OR = 2.6, 95% Cl 1.2-5.6) and textile industries (OR = 2.5, 95% Cl 1.3-4.7). Several toxic agents were associated with risk elevation of 1.3 or greater for fathers, most notably benzene (OR = 1.5, 95% Cl 1.1-2.3). In spite of limitations in the exposure data, the size of the exposed populations, and possible confounding, the results in this study encourage further evaluation of the effects of maternal exposure to lead and possibly solvents, as well as paternal exposure in the textile industry and to x-rays and benzene.     

The contribution of acute toxicity in animals to occupational exposure limits of chemical substances

The correlations of lethal doses of various industrial chemicals for rats and mice with occupational exposure limit values were investigated. 50% lethal dose (LD50) values obtained by oral (p.o.) and intraperitoneal (i.p.) injection and 50% lethal concentration (LC50) values obtained by inhalation exposure were collected from Registry of Toxic Effects of Chemical Substances (RTECS). Threshold Limit Value (Time-Weighted Average) (TLVs-TWA) and Threshold Limit Value (Short Term Exposure Limit) (TLVs-STEL) recommended by American Conference of Governmental Industrial Hygienists (ACGIH) were used as exposure limits. TLVs-TWA or TLVs-STEL and LD50 or LC50 values obtained for the rats were plotted on logarithmic scales on the ordinate and abscissa, respectively. High correlations were obtained between these parameters. The order of correlations was: TLVs-STEL vs. LC50s > TLVs-TWA vs. LC50s > TLVs-TWA vs. LD50s i.p. > TLVs vs. LD50s p.o. The same calculations for the relationship between TLVs and lethal doses in mice were also performed. The order of the three types of correlations was same as that of the rats; however, correlation coefficients for TLVs-STEL vs. LC50s and for TLVs-TWA vs. LC50s obtained in mice were smaller than those in rats. TLVs-TWA are, therefore, well correlated with LC50 values rather than LD50 values, particularly with those in rats. High correlations between TLVs-STEL vs. LC50s were also obtained, as had been expected before calculation. The equation: TLV-TWA = 10b x (LC50)a can be obtained from these plottings, where the values a and b are taken from each linear regression line. TLV-TWA for each chemical can be calculated by using LC50 and the equation. The upper and lower 95% confidence limits for calculated TLV-TWA were TLV-TWA (calculated from LC50) x 22.9 and TLV-TWA (calculated)/22.9, respectively, where LC50 for rats expressed in ppm x hr was used.     

某化工企业职业接触苯致癌风险评估

检测某化工企业作业场所空气中的苯浓度,确定高毒物质苯危害的风险等级,建立苯接触致癌风险剂量-反应模型,提出相应风险的防控措施。结果显示,苯乙烯生产装置中苯所致职业病危害为高风险等级,操作工、质检工职业接触苯的致癌风险分别为 0.55×10^-4、0.39×10^-4,属于可接受风险水平。长期低浓度苯接触存在的潜在风险不容忽视。     

Reducing occupational exposure to chemical carcinogens

Strategies for controlling occupational exposure to chemicalcarcinogens are set out in the European Union Carcinogens Directiveand in national legislation such as the British Control of SubstancesHazardous to Health Regulations. While such legislative requirementsmust apply to all occupational chemical carcinogens, it is arguedthat priority should be given to controlling those agents thatcontribute most to the cancer burden. Examples of possible strategiesto reduce exposure to two agents (diesel exhaust particulateand paint emissions) are discussed. It is concluded that thereare no real technical difficulties in controlling exposuresto chemical carcinogens; however, for many of the key agents,we need to change attitudes to the potential risks and clearlydemonstrate to employers and employees how to reduce the exposures.     

A case-control study of brain gliomas and occupational exposure to chemical carcinogens: the risk to farmers

During 1983 and 1984, 240 newly diagnosed cases of brain glioma and 742 controls (465 non-glioma nervous system tumors and 277 patients with other neurologic diseases) were recruited and interviewed in the neurologic and neurosurgical departments of two hospitals in Milan, Italy. The occupational histories of cases and controls were compared, and relative risk estimates, adjusted for sex, age, residence, and socioeconomic status, were computed using the Mantel-Haenszel method. A statistically significant risk increase was found for farmers (relative risk (RR) = 1.6, p = 0.0025). This risk increase was attributable to those farmers who reported the use of chemicals (insecticides or fungicides, herbicides, and fertilizers). Among the three groups of investigated agrochemicals, only the use of insecticides or fungicides was associated with a significant increase in relative risk (RR = 2.0, p = 0.006). Many farmers exposed to fungicides reported the use of commercial compounds of copper sulfate. Some of these compounds contain methyl urea, which has a specific carcinogenic effect on the nervous system in animals. These data suggest that the occupational exposure of farmers to agrochemicals might be responsible for the observed excess risk of brain glioma in farmers.     

Maternal occupational and hobby chemical exposures as risk factors for neural tube defects

In a case-control study, we investigated whether occupational and nonoccupational (hobbies) chemical exposures to women in the periconceptional period increased their risk for having neural tube defect-affected pregnancies. Women were asked about occupational tasks and hobbies performed during the 3 months before through 3 months after conception. Based on her reported occupational tasks and hobbies, an industrial hygienist assigned a priori defined exposure categories to each task and hobby. The exposure categories included 74 chemical groups, 9 "end-use" chemical groups, and organic solvents. Face-to-face interviews were conducted with mothers of 538 (88% of eligible) infants or fetuses with neural tube defect and mothers of 539 (88%) randomly selected, nonmalformed, live-born infants from a population-based 1989-1991 cohort of California births (N = 703,518). Our results suggested that maternal exposures in the periconceptional period to a variety of chemicals associated with occupational and nonoccupational activities did not contribute substantially to risk of neural tube defects in offspring. We observed no effect estimate greater than 2.0 for maternal exposures to the chemical agent groups studied. We did not observe substantially elevated risks associated with maternal exposures to any of the end-use chemical groups or to organic solvents. Considering occupational exposures only among women who worked did not substantially alter results. Adjustment for maternal vitamin use, race/ethnicity, or education level also did not substantially alter the observed associations.     

Soft-tissue sarcomas and exposure to chemical substances: a case-referent study.

In 1977 several patients were seen with soft-tissue sarcomas and previous exposure to phenoxy acids. This clinical observation resulted in a cases-referent (case-control) study being undertaken which showed that exposure to phenoxy acids or chlorophenols, which are chemically related, gave a roughly six-fold increase in the risk for this type of tumour. A further case-referent study of soft-tissue sarcomas has now been performed to confirm these earlier findings and also to obtain further information on the effects of different phenoxy acids. This new investigation gave an increase of the same magnitude in the risk for soft-tissue sarcomas after exposure to phenoxy acids or chlorophenols, but this risk related also to exposure to phenoxy acids free from impurities, such as polychlorinated dibenzodioxins and dibenzofurans.     

Interactions between alcohol and work exposure to chemical substances

BACKGROUND AND OBJECTIVES: The quite diffused habit of a significant assumption of alcohol drinks, can interfere with the professional exposure to chemical substances. The interaction may result in increasing their toxicity and/or modifying the parameters of the biological monitoring. It may also act as a confounding factor, not only in epidemiologic researches but also at individual level when the assessment of the occupational exposure and/or the diagnosis of an occupational diseases, is under consideration. We review available references in the literature summarizing major scientific evidences. RESULTS: The interaction between the alcohol assumption and industrial chemicals may be toxicokinetic or toxicodynamic. Alcohol can interfere in the processes of biotransformation of xenobiotics and modify the doses and the effect indicators used for the biological monitoring, causing wrong interpretations of the results. The metabolism of ethanol can be altered by the exposures to toxic industrial materials, creating some clinical pictures of alcohol intolerance, like an "antabuse syndrome" or an "degreaser flush syndrome". Professional exposure to carbon sulfide or to dimethylformamides, trichloroethylene as well as to nitroglycerin and nitroglycole ethylenic can produce similar syndromes. Interactions are reported between alcohol and solvents: on toxicokinetic bases for methanol, isopropanol, glycol ether, trichloroethylene, methyl ethyl ketone and toluene; and on toxicodynamic bases for CNS. Also between alcohol and metals there can occur toxicokinetic interactions, like in the case of lead and mercury. Alcohol can also interfere with the biological monitoring of solvents, producing an over-estimation of the exposure. CONCLUSIONS: For the biological monitoring of reported chemical substances, it is suitable to evaluate the biologic indicators in the days in which there is not assumed alcohol. If this cannot be guaranteed, it is necessary to know at least the quantity of the alcohol consumed or at least if the subject is an alcohol abuser.