Maternal Occupational Exposure Research Articles

Environmental pollution and the development of congenital heart disease: A scoping review

Introduction: Congenital heart disease (CHD) is the most common congenital anomaly in infancy affecting 1% of all live births worldwide of which the etiology in most affected children is unknown. The role of environmental pollutants from various sources is increasingly gaining attention. To explore the existing breadth of knowledge on this topic, we undertook a scoping review of studies examining the role of environmental pollution in relation to the development of CHD. Methods: We searched various databases for studies reporting CHD and exposures to chemicals using Medical Subject Headings (MeSH) and non-MeSH including criteria pollutants (e.g. CO, SO2 NO2), occupational, non-occupational, industrial chemicals and emissions reported in pollutant release and transfer registries (PRTR) from 1980 to 2018. Results: We identified 70 studies that were grouped into the categories of outdoor industrial chemical pollution; urban air pollution; occupational; and non-occupational exposures. There were no marked differences in proportions of studies in the first three categories, which ranged between 29-33%. Non-occupational exposures accounted for 7% of the studies. Proximity to industrial facilities and hazardous waste sites was associated with CHD in a modest number of studies that used PRTR. Urban criteria pollutants were consistently associated with CHD. Maternal occupational exposures were more commonly studied compared to paternal exposures and organic solvents were associated with CHD in these studies. There were limited studies that examined non-occupational and multipollutant exposures. Conclusion: We identified associations between various chemicals and CHD, employing diverse methods of exposure assessment. Most studies examined single pollutant exposures and have demonstrated inconclusive findings. Future studies should examine multiple pollutant exposures and CHD. In addition to monitored data, exploratory studies could exploit PRTR in countries where such registries exist. Furthermore, multicenter studies that examine larger populations of affected patients could facilitate the discovery of the relationship between specific chemicals and CHD subtypes.

Risk Factors Associated with Juvenile Idiopathic Arthritis: Exposure to Cigarette Smoke and Air Pollution from Pregnancy to Disease Diagnosis.

To evaluate exposure to environmental factors inhaled during pregnancy and after birth until juvenile idiopathic arthritis (JIA) diagnosis among residents of a large city. This is an exploratory case-control study that consists of 66 patients with JIA and 124 healthy controls matched by age and sex, living in the São Paulo, Brazil, metropolitan area until JIA diagnosis, and whose mothers had resided in this region during pregnancy. A structured and reliable questionnaire (κ index for test-retest was 0.80) assessed demographic data, gestational and perinatal-related factors, and exposure to inhalable environmental elements during pregnancy and after birth (occupational exposure to inhalable particles and/or volatile vapor, exposure to cigarette smoke, and the presence of industrial activities or gas stations near the home, work, daycare, or school). Tropospheric pollutants included particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and carbon monoxide (CO). During pregnancy, intrauterine cigarette smoke exposure (OR 3.43, 95% CI 1.45-8.12, p = 0.005) and maternal occupational exposure (OR 13.69, 95% CI 4.4-42.3, p < 0.001) were significant independent risk factors for JIA diagnosis. In contrast, maternal employment (OR 0.06, 95% CI 0.02-0.2, p < 0.001) and ideal maternal weight gain (OR 0.36, 95% CI 0.2-0.8, p = 0.017) presented negative associations. Secondhand smoke exposure from birth to JIA diagnosis (OR 3.6, 95% CI 1.8-7.3, p < 0.001) and exposure to O3 during the second year of life (OR 2.76, 95% CI 1.20-6.37, p = 0.017) were independent and significant risk factors for the pathogenesis of JIA. In our study, cigarette smoke exposure (intrauterine and after birth), exposure to O3 in the second year of life, and maternal occupational exposure were identified as potential risk factors for JIA, warranting further study.

Mother and child characteristics at birth and early age leukemia: a case‐cohort population‐based study

ObjectiveThe population‐based cancer registries (PBCR) and the Information System on Live Births in Brazil (Sistema de Informações sobre Nascidos Vivos [SINASC]) have information that enables the test for risk factors associated with leukemia at an early age. The aim of this study was to identify maternal and birth characteristics associated with early‐age acute leukemia (EAL) in Brazil. MethodsA case‐cohort study was performed using secondary dataset information of PBCR and SINASC. The risk association variables were grouped into (i) characteristics of the child at birth and (ii) characteristics of maternal exposure during pregnancy. The case–control ratio was 1:4. Linkage was performed using R software; odds ratio (OR) and 95% confidence interval (CI) were calculated by logistic regression models. ResultsEAL was associated with maternal occupational exposure to chemicals (agricultural, chemical, and petrochemical industry; adjOR: 2.18, 95% CI: 1.16–4.10) and with birth defects (adjOR: 3.62, 95% CI: 1.19–11.00). ConclusionsThe results of this study, with the identification of EAL risk factors in population‐based case‐cohort study, strengthen the knowledge and improve databases, contributing to investigations on risk factors associated with childhood leukemia worldwide.

Congenital heart defects of fetus after maternal exposure to organic and inorganic environmental factors: a cohort study.

ObjectiveMaternal exposure to various contaminants has been reported to be correlated with congetinal heart defects (CHDs). In this study, the effect of maternal exposure to organic and inorganic environmental factors upon the incidence of CHDs was investigated. We conducted a retrospective birth cohort study of infants born in the Maternal and Child Health Hospital of Panyu District in Guangzhou.Materials and MethodsA total of 5381 cases with complete medical records, including mothers, fathers, and infants, were enrolled. The relationship between maternal occupational exposure to hazardous substances and strong noise during pregnancy and CHDs was analyzed. Occupational exposure to hazardous substances increased the incidence of CHDs.ResultsForty-eight of 145 mothers (33.1%) in the CHDs group worked in hazardous and strong noise factories, while the corresponding percentage mothers in the control group was 22.8% (1193/5236). The percentage of mothers with a history of contact with organic solvents and exposure to strong noise in the CHDs group was significantly higher than the control group. There was no significant difference in the histories of contact with heavy metals, high temperatures, and other extreme environments between two groups.ConclusionsHazardous substances in factories, especially organic solvents, were identified as potential risk factors for CHDs. Besides, exposure to high noise also increased the incidence of CHDs.

Maternal occupational exposure and oral clefts in offspring

BackgroundPrevious studies suggest that periconceptional maternal occupational exposure to solvents and pesticides increase the risk of oral clefts in the offspring. Less is known about the effect of occupational exposure to metals, dust, and gases and fumes on development of oral clefts.MethodsThis case-malformed control study used data from a population-based birth defects registry (Eurocat) of children and foetuses born in the Northern Netherlands between 1997 and 2013. Cases were defined as non-syndromic oral clefts. The first control group had chromosomal/monogenic defects, and the second control group was defined as non-chromosomal/non-monogenic malformed controls. Maternal occupational exposure was estimated through linkage of mothers’ occupation with a community-based Job Exposure Matrix (JEM). Multivariate logistic regression was used to estimate the effect of occupational exposures. Odds ratios were adjusted (aORs) for relevant confounders.ResultsA total of 387 cases, 1135 chromosomal and 4352 non-chromosomal malformed controls were included in this study. Prevalence of maternal occupational exposures to all agents was 43.9% and 41.0%/37.7% among cases and controls, respectively. Oral clefts had significantly increased ORs of maternal occupational exposure to pesticides (aOR = 1.7, 95% confidence interval [CI] 1.0–3.1) and dust (aOR = 1.3, 95% CI 1.1–1.6) when using non-chromosomal controls. Subgroup analysis for CL(P) stratified by gender showed a significantly increased risk for male infants exposed to ‘other solvents’ and exposure to mineral dust for female infants.ConclusionOur study showed that maternal occupational exposure to pesticides and dust are risk factors for oral clefts in the offspring. Larger studies are needed to confirm this finding.

Mother and child characteristics at birth and early age leukemia: a case-cohort population-based study

ObjectiveThe population-based cancer registries (PBCR) and the Information System on Live Births in Brazil (Sistema de Informações sobre Nascidos Vivos [SINASC]) have information that enables the test for risk factors associated with leukemia at an early age. The aim of this study was to identify maternal and birth characteristics associated with early-age acute leukemia (EAL) in Brazil. MethodsA case-cohort study was performed using secondary dataset information of PBCR and SINASC. The risk association variables were grouped into (i) characteristics of the child at birth and (ii) characteristics of maternal exposure during pregnancy. The case–control ratio was 1:4. Linkage was performed using R software; odds ratio (OR) and 95% confidence interval (CI) were calculated by logistic regression models. ResultsEAL was associated with maternal occupational exposure to chemicals (agricultural, chemical, and petrochemical industry; adjOR: 2.18, 95% CI: 1.16–4.10) and with birth defects (adjOR: 3.62, 95% CI: 1.19–11.00). ConclusionsThe results of this study, with the identification of EAL risk factors in population-based case-cohort study, strengthen the knowledge and improve databases, contributing to investigations on risk factors associated with childhood leukemia worldwide.

Are prematurity and environmental factors determinants for developing childhood-onset systemic lupus erythematosus?

Objective: The objective of this study is to evaluate the influence of exposure to air pollutants and inhalable environmental elements during pregnancy and after birth until childhood-onset systemic lupus erythematosus(cSLE) diagnosis.Methods: This case–control study comprised 30 cSLE patients and 86 healthy controls living in the Sao Paulo metropolitan area. A structured and reliable questionnaire (kappa index for test-retest was 0.78) assessed demographic data, gestational and perinatal-related-factors, and exposure to inhalable elements during pregnancy and after birth (occupational exposure to inhalable particles and/or volatile vapor, and/or tobacco, as well as, the presence of industrial activities or gas stations near the home/work/daycare/school). Tropospheric pollutants included: particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3) and carbon monoxide (CO).Results: The median current age was similar between cSLE patients and healthy controls [16.0 (5–21) versus 15.0 (4–21) years, p = .32], likewise the frequency of female gender (87% versus 78%, p = .43). The frequencies of prematurity (30% versus 6%, p = .001), maternal occupational exposure during pregnancy (59% versus 12%, p < .001), exposure to volatile vapor (48% versus 8%, p < .001) and fetal smoking (maternal and/or secondhand) (37% versus 19%, p = .008) were significantly higher in cSLE patients compared with controls. In a multivariate analysis regarding the gestation period, maternal occupational exposure (OR 13.5, 95% CI 2.5–72.4, p = .002), fetal smoking (OR 8.6, 95%CI 1.6–47, p = .013) and prematurity (OR 15.8, 95%CI 1.9–135.3, p = .012) remained risk factors for cSLE development. Furthermore, exposure to secondhand smoking during pregnancy and after birth (OR 9.1, 95%CI 1.8–42.1, p = .002) was also a risk factor for cSLE development.Conclusions: Prematurity and environmental factors were risk factors for developing cSLE.

Parental Occupational Exposure to Organic Solvents and Testicular Germ Cell Tumors in their Offspring: NORD-TEST Study.

Background:Testicular germ cell tumors (TGCT) were suggested to have a prenatal environmentally related origin. The potential endocrine disrupting properties of certain solvents may interfere with the male genital development in utero.Objectives:We aimed to assess the association between maternal and paternal occupational exposures to organic solvents during the prenatal period and TGCT risk in their offspring.Methods:This registry-based case control study included TGCT cases aged 14–49 y () diagnosed from 1978 to 2012 in Finland, Norway, and Sweden. Controls () were randomly selected from the central population registries and were individually matched to cases on year and country of birth. Occupational histories of parents prior to the child’s birth were extracted from the national censuses. Job codes were converted into solvent exposure using the Nordic job-Nordic Occupational Cancer Study Job-Exposure Matrix. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI).Results:Overall, no association was found between prenatal maternal exposure to solvents and TGCT risk. In subset analyses using only mothers for whom occupational information was available in the year of or in the year prior to the child’s birth, there was an association with maternal exposure to aromatic hydrocarbon solvents (ARHC) (; CI: 1.08, 2.17), driven by exposure to toluene (; CI: 1.02, 2.73). No association was seen for any paternal occupational exposure to solvents with the exception of exposure to perchloroethylene in Finland (; CI: 1.32, 4.41).Conclusions:This study suggests a modest increase in TGCT risk associated with maternal prenatal exposure to ARHC. https://doi.org/10.1289/EHP864

Glycol Ethers and Neurodevelopment: Investigating the Impact of Prenatal Exposures.

Vol. 125, No. 6 Science SelectionsOpen AccessGlycol Ethers and Neurodevelopment: Investigating the Impact of Prenatal Exposures Nate Seltenrich Nate Seltenrich Search for more papers by this author Published:22 June 2017CID: 064001https://doi.org/10.1289/EHP2094View Article in:中文版AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit Glycol ethers have been widely used since the 1960s as solvents and stabilizers in a variety of personal, household, and industrial products.1 A new study in Environmental Health Perspectives provides some of the first evidence of associations between prenatal exposures to glycol ethers and cognitive impairments in children.2These chemicals are generally valued for their low acute toxicity. However, the European Union has restricted3 the use of several glycol ethers due to concerns about potential reproductive toxicity and other health risks.1In the current study, researchers in France measured five glycol ether metabolites in urine samples from 204 pregnant women, which had been collected between 2002 and 2006 for the broader PELAGIE mother–child cohort.4 At age 6, their children were given a series of neurocognitive tests to assess verbal comprehension, working memory, and visuospatial ability.All the women had detectable levels in their urine of the metabolites phenoxyacetic acid (PhAA) and 2-butoxyacetic acid (BAA, a by-product of two restricted glycol ethers used in hair dyes and spray paints and cleaners). Nearly all women also had detectable levels of ethoxyacetic acid (EAA), ethoxyethoxyacetic acid (EEAA), and methoxyacetic acid (MAA). The authors note that this high frequency of detection and the relatively short half-life of these metabolites in the body (6–80 hours) suggest that exposures are not only common but also repeated.2After adjusting for potential confounders, including the mother’s intelligence and the amount of cognitive and emotional stimulation the child received at home, the researchers found that higher verbal comprehension scores among the children were associated with lower levels of PhAA in their mothers’ urine during pregnancy. PhAA is the primary metabolite of 2-phenoxyethanol (EGPhE), a glycol ether commonly used in perfumes, cosmetics, lotions, and other personal care products.2Glycol ethers are excreted relatively quickly, so when studying the health effects of these compounds, it matters when samples are collected. First-morning urine samples, for instance, would not capture glycol ether exposures from products used during the day. © ShotShare/iStockphoto.The researchers also reported a weaker association between a mother’s urinary levels of EAA in pregnancy and her child’s ability to copy simple drawings.2 This compound is a metabolite of glycol ethers commonly used in cleaning products.Lead author Rémi Béranger, a midwife and postdoctoral researcher with the French National Institute of Health and Medical Research, is not aware of any previous studies in this area. “We strongly need other studies to investigate the same question, because the evidence is insufficient right now,” he says. “I know that researchers always say that, but because of the limited evidence of biological plausibility we really need additional studies.”The authors note several limitations. For one, they had only a single urine sample per woman, offering limited information because glycol ether metabolites clear from the body relatively rapidly. Urine samples collected upon waking, for instance, would not capture exposures resulting from applying cosmetics later in the morning.2In addition, the results possibly could be explained by exposure to preservatives or other chemicals often used in conjunction with glycol ethers,2 including parabens, sodium benzoate, and methyldibromoglutaronitrile.5 Little is known about whether exposures to these chemicals may be associated with neurodevelopmental outcomes in the children of mothers with such exposures.Studies of prenatal exposure to organic solvents in general (as opposed to glycol ethers in specific, which are one group in the larger family) have found higher maternal occupational exposure during pregnancy to be associated with reduced visual ability6,7 and neurobehavioral performance8,9 in children. Another study reported a relationship between organic solvent exposure and visual–motor ability, the same skill shown in the present study to be slightly depressed in children whose mothers had the highest urinary levels of EAA.10York University professor Christine Till, lead author of the latter paper, says that the new work by Béranger et al. is “a direct replication of what we were finding.” She adds, “I was impressed overall by the methodology, and it is interesting to see the findings replicate what we reported.”Future research into possible neurodevelopmental toxicity of glycol ethers should target potential mechanisms, such as oxidative stress and impacts on neurotransmitters, as well as [provide] better understanding of how populations are exposed to the chemicals, says senior author and PELAGIE principal investigator Cecile Chevrier.The study also highlights the need for more research into cognitive outcomes associated with early life chemical exposures in general, according to Paule Vasseur, professor at France’s University of Lorraine, who was not involved in the study. “The consequences of chemical exposure during pregnancy are very poorly known, and the chemicals responsible for neurocognitive effects sparsely identified,” she says. “This is a goal for the coming years.”

Parental exposures to occupational asthmagens and risk of autism spectrum disorder in a Danish population-based case-control study

BackgroundEnvironmental exposures and immune conditions during pregnancy could influence development of autism spectrum disorder (ASD) in offspring. However, few studies have examined immune-triggering exposures in relation to ASD. We evaluated the association between parental workplace exposures to risk factors for asthma (“asthmagens”) and ASD.MethodsWe conducted a population-based case-control study in the Danish population using register linkage. Our study population consisted of 11,869 ASD cases and 48,046 controls born from 1993 through 2007. Cases were identified by ICD-10 codes in the Danish Psychiatric Central Register. ASD cases and controls were linked to parental Danish International Standard Classification of Occupations (DISCO-88) job codes. Parental occupational asthmagen exposure was estimated by linking DISCO-88 codes to an asthma-specific job-exposure matrix.ResultsOur maternal analyses included 6706 case mothers and 29,359 control mothers employed during the pregnancy period. We found a weak inverse association between ASD and any maternal occupational asthmagen exposure, adjusting for sociodemographic covariates (adjusted OR: 0.92, 95% CI: 0.86–0.99). In adjusted analyses, including 7647 cases and 31,947 controls with employed fathers, paternal occupational asthmagen exposure was not associated with ASD (adjusted OR: 0.98, 95% CI: 0.92–1.05).ConclusionsWe found a weak inverse association between maternal occupational asthmagen exposure and ASD, and a null association between paternal occupational exposure and ASD. We suggest that unmeasured confounding negatively biased the estimate, but that this unmeasured confounding is likely not strong enough to bring the effect above the null. Overall, our results were consistent with no positive association between parental asthmagen exposure and ASD in the children.

A task-based assessment of parental occupational exposure to pesticides and childhood acute lymphoblastic leukemia

ObjectivesAssociations between parental occupational pesticide exposure and childhood acute lymphoblastic leukemia (ALL) vary across studies, likely due to different exposure assessment methodologies. MethodsWe assessed parental occupational pesticide exposure from the year before pregnancy to the child's third year of life for 669 children diagnosed with ALL and 1021 controls. We conducted expert rating using task-based job modules (JM) to estimate exposure to pesticides among farmer workers, gardeners, agricultural packers, and pesticide applicators. We compared this method to (1) partial JM using job titles and a brief description, but without completing the task-based questionnaire, and (2) job exposure matrix (JEM) linking job titles to the International Standard Classifications of Occupation Codes. We used unconditional logistic regression to calculate odds ratios (OR) and 95% confidence intervals (95% CI) for ALL cancer risk and pesticide exposure adjusting for child's sex, age, race/ethnicity and household income. ResultsCompared to complete JMs, partial JMs and JEM led to 3.1% and 9.4% of parents with pesticide exposure misclassified, respectively. Misclassification was similar in cases and controls. Using complete JMs, we observed an increased risk of ALL for paternal occupational exposure to any pesticides (OR=1.7; 95% CI=1.2, 2.5), with higher risks reported for pesticides to treat nut crops (OR=4.5; 95% CI=0.9, 23.0), and for children diagnosed before five years of age (OR=2.3; 95% CI: 1.3, 4.1). Exposure misclassification from JEM attenuated these associations by about 57%. Maternal occupational pesticide exposure before and after birth was not associated with ALL. ConclusionsThe risk of ALL was elevated in young children with paternal occupational pesticide exposure during the perinatal period, using more detailed occupational information for exposure classification.

Maternal and paternal occupational exposures and hepatoblastoma: results from the HOPE study through the Children's Oncology Group.

Little is known about the etiology of hepatoblastoma. We aimed to confirm the results of a previous study evaluating the association between parental occupational exposures and hepatoblastoma. In our case-control study, we identified cases (n=383) from the Children's Oncology Group and controls from birth certificates (n=387), which were frequency matched to cases on year and region of birth, sex, and birth weight. Occupational exposure in the year before and during the index pregnancy was collected through maternal interview and analyzed using unconditional logistic regression. The odds of both paternal and maternal "Likely" exposure to paints was elevated among cases compared with controls (paternal odds ratio (OR): 1.71, 95% confidence interval (CI): 1.04, 2.81; maternal OR: 3.29, 95% CI: 0.32, 33.78) after adjustment for matching factors and the confounding factors of maternal race (maternal only) and household income. In addition, paternal exposure to other chemicals was also elevated when adjusting for matching factors only (OR: 1.53, 95% CI: 1.02, 2.30). The results of our study provide further evidence of an association between parental occupation and hepatoblastoma. These results warrant further investigation of the etiologically relevant timing of occupational exposure to fumes and chemicals related to hepatoblastoma.

Maternal Exposure to Domestic Hair Cosmetics and Occupational Endocrine Disruptors Is Associated with a Higher Risk of Hypospadias in the Offspring.

Pregnant women are exposed to various chemical products at home and at work. Some of these products contain endocrine-disrupting chemicals (EDCs) such as cosmetics, pesticides, industrial chemicals, heavy metals, plastics or medications that could alter sexual differentiation and increase the risk of hypospadias. We evaluated maternal occupational and household exposures that could constitute risk factors for hypospadias. From 2011 to 2014, we enrolled 57 full-term newborns with hypospadias and three randomly selected controls per case (162 control newborns), matched for gestational age, from 11 maternity units in Picardy, France. Neonatal and parental data were collected at birth (personal characteristics, maternal lifestyle, and medical history). Maternal occupational exposure was assessed by a job-exposure matrix for EDCs from a job history questionnaire completed by mothers. Odds ratios (OR) and 95% confidence intervals (CI) were calculated with univariate and multivariable logistic regression, and adjusted for relevant covariates. Multivariate analysis showed a strong association between hypospadias and potential maternal occupational exposure to EDCs and maternal household use of hair cosmetics (OR 6.1, 95% CI: 1.1–34.9; OR: 9.6, 95% CI: 1.4–66.1, respectively). Our results suggest that maternal occupational exposure to EDCs is a risk factor for hypospadias and suggests a possible influence of household use of hair cosmetics during early pregnancy on the incidence of hypospadias in the offspring. A larger study with more accurate exposure assessment should evaluate the impact of EDCs in hair cosmetics on the incidence of hypospadias.

A discriminant analysis prediction model of non-syndromic cleft lip with or without cleft palate based on risk factors.

BackgroundA risk prediction model of non-syndromic cleft lip with or without cleft palate (NSCL/P) was established by a discriminant analysis to predict the individual risk of NSCL/P in pregnant women.MethodsA hospital-based case–control study was conducted with 113 cases of NSCL/P and 226 controls without NSCL/P. The cases and the controls were obtained from 52 birth defects’ surveillance hospitals in Hunan Province, China. A questionnaire was administered in person to collect the variables relevant to NSCL/P by face to face interviews. Logistic regression models were used to analyze the influencing factors of NSCL/P, and a stepwise Fisher discriminant analysis was subsequently used to construct the prediction model.ResultsIn the univariate analysis, 13 influencing factors were related to NSCL/P, of which the following 8 influencing factors as predictors determined the discriminant prediction model: family income, maternal occupational hazards exposure, premarital medical examination, housing renovation, milk/soymilk intake in the first trimester of pregnancy, paternal occupational hazards exposure, paternal strong tea drinking, and family history of NSCL/P. The model had statistical significance (lambda = 0.772, chi-square = 86.044, df = 8, P < 0.001). Self-verification showed that 83.8 % of the participants were correctly predicted to be NSCL/P cases or controls with a sensitivity of 74.3 % and a specificity of 88.5 %. The area under the receiver operating characteristic curve (AUC) was 0.846.ConclusionsThe prediction model that was established using the risk factors of NSCL/P can be useful for predicting the risk of NSCL/P. Further research is needed to improve the model, and confirm the validity and reliability of the model.

Risk of Central Nervous System Tumors in Children Related to Parental Occupational Pesticide Exposures in three European Case-Control Studies.

The aim of this study was to assess the risk of childhood central nervous system (CNS) tumors associated with parental occupational pesticide exposure. We pooled three population-based case-control studies from France, Germany, and the United Kingdom. Cases were children below 15 years of age with CNS tumors; controls were matched by gender and age. A general population job-exposure matrix assessed parental occupational pesticide exposure. Logistic regressions estimated odds ratios (ORs) and 95% confidence intervals (CIs). The study included 1361 cases and 5498 controls. Prevalence of maternal occupational pesticide exposure during pregnancy was low and no association with childhood CNS tumors was detected (OR 0.76, 95% CI: 0.41 to 1.41). Around conception, OR for childhood CNS tumors associated with paternal occupational pesticide exposure was 0.71 (95% CI: 0.53 to 0.95). Our results do not suggest a role of parental occupational pesticide exposure in the etiology of childhood CNS tumors.

Increased time-to-pregnancy is associated with domestic work in South Africa.

BackgroundThe effects of female occupational exposures on fecundity have not been evaluated in South Africa. The aim of this study was to assess the effects of three specific occupational groups on time-to-pregnancy (TTP).MethodsThis cross-sectional study collected data, by means of a questionnaire, on 1210 women representative of a South African population, and sought information on: TTP for the most recent pregnancy, time-specific information on maternal factors and occupational exposures, as well as some paternal factors. Occupational exposure groups were determined using employment profile prior to the pregnancy. In the risk analysis, domestic workers and teachers were compared to administrative staff. Accidental and unplanned pregnancies were excluded from the analysis and participants who were never pregnant were censored. Discrete-time Cox regression models were built to estimate fecundability ratios (FR).ResultsThe median TTP in administrative workers, domestic workers and teachers was 4, 12 and 3 months respectively. After adjusting for a number of potential confounders, TTP was significantly related to occupation at the time of pregnancy attempt. Compared to administrative workers, domestic workers had a significantly lower per-cycle probability of conception (adjusted FR = 0.53; 95 CI 0.32–0.88). The per-cycle probability of conception in teachers compared to administrative workers was not significantly different (adjusted FR = 1.14; 95 CI: 0.75–1.72).ConclusionDomestic work was associated with prolonged TTP. Working as a domestic worker in South Africa may affect fecundity.

Maternal Occupational Exposure and Breastfeeding Impact on Programming Child Allergy

Introduction. Epidemiologic data suggest a possible association between maternal exposure to chemical substances and risk of childhood allergy in offspring. The overall beneficial effects of breastfeeding for infants’ growth, immunity, and development have been well documented, but its role in allergy prevention is controversial. The purpose of this study was to assess the effect of maternal occupational exposure to chemical substances on programming allergy in 4–6 years children and to evaluate breastfeeding impact on these associations. Methods. This nested cases-control study included 645 mother-children pairs. Allergy was assessed by the standardized questionnaires. Logistic regression models were fitted to examine the associations as odds ratios (OR) between maternal occupational exposure, breastfeeding duration and the risk of allergy adjusted for relevant covariates. Results. As many as 67.0% of the mothers reported having occupational exposure to chemical substances more than 1 year before pregnancy. Children of mothers exposed at work to chemical substances had increased prevalence of allergy at 4–6 years age comparing with not exposed (32.6% and 25.0%, accordingly). Occupationally exposed to chemical substances mothers breastfeeding more than 3 months increased 4–6 years children allergy risk by 59 %, adjusted OR 1.59; 95% CI 0.80–3.16. These associations were robust to adjustment for covariates associated with allergy, such as maternal education, smoking during pregnancy, chronic disease, child’s gender, and low birth weight. Conclusions. Occupationally exposed to chemical substances mothers’ breastfeeding may be a predictor of allergy throughout the developmental trajectory of childhood. Further investigation is needed to elucidate the influence of chemical substances and breastfeeding on childhood allergy.

Prenatal exposure to chemical products, early indoor environment and wheezing and eczema in infancy

Home environment has been linked to childhood allergies and asthma, as have been several household chemical products, but evidence on their health effects in early life is scarce. We aimed to explore associations of prenatal exposure to chemical substances and indoor environmental exposures in the first months of life with wheezing and eczema in infancy. The study included 4422 singletons from the Italian NINFEA birth cohort. Maternal occupational or non-occupational exposure to chemical products in the third trimester of pregnancy and indoor environment in the first 6 months of life were ascertained from the questionnaire completed by mothers at 6 months of age. Information on the occurrence of wheezing and eczema between 6 and 18 months of age was obtained from the questionnaire completed 18 months after delivery. Analyses were adjusted for maternal age, history of asthma and atopy, educational level, nationality, smoking during pregnancy and parity. Infant wheezing and eczema prevalence were 17.6% and 16.3%, respectively. The most commonly used chemical products in the third trimester were bleach (39.8%), disinfectants (39.4%) and window-cleaning products (35.4%). Maternal use of insecticides/pesticides was associated with wheezing (adjusted OR: 1.44; 95%CI: 1.02-2.03), while use of bleach (1.30; 1.11-1.53), paint remover (2.12; 1.07-4.20) and adhesives/mastics (1.47; 1.05-2.06) was associated with infant eczema. Analyses restricted to frequent use (≥1 per week) revealed additional associations between window-cleaning products and eczema, and wall paint and wheezing. Day-care attendance, urban living area, dampness/mould and cooking with gas in the first 6 months of life were positively associated with infant wheezing. Of these exposures, only urban living area was associated with eczema (0.72; 0.59-0.89). These data suggest that several environmental exposures during a critical developmental period are involved in the onset of early wheezing and eczema.

Occupational solvent exposures during pregnancy and child behavior at age 6: The PELAGIE cohort study

Introduction: We previously found prenatal solvent exposures at higher risk of externalizing disorders in 2-year-old children, consistently with animal data and the few existing study in human. We aimed to assess the impact of maternal occupational exposure to solvents during pregnancy on the children behavior until age 6, within the PELAGIE cohort. Methods: Maternal occupational exposure to solvents was assessed using job-exposure matrices (JEM) and self-reported items at early pregnancy. Children’s behavior was assessed using the Strength and Difficulties Questionnaire at age 6 (n=1264) and items derived from the Child Behavior Checklist at age 2 (n=833). Trajectories of externalizing disorders (hyperactivity and conduct problems) from age 2 to 6 were determined using k-means clustering methods. Poisson and logistic regression models were performed. Results: We found increased internalizing (emotional and peer-relationship) and externalizing disorders at age 6 among children of women self-reporting occasional (beta = 0.11 [CI95% 0.00, 0.23]; 0.09 [-0.01, 0.20], respectively), but not regular exposure to solvents during pregnancy. Based on JEM, internalizing disorders among children of women exposed to petroleum solvents tended to increase (beta=0.09 [-0.01, 0.19]). Four trajectories of externalizing disorders were identified (high-high; high-low; low-high and low-low, lower is better). Children of women self-reporting occasional exposure to solvents during pregnancy had more often high (age 2)-high (age 6) and high-low trajectories of conduct problems (reference: low-low, OR=2.03 [1.08, 3.82]; 2.15 [1.23, 3.76], respectively). No association was observed with regular exposures. Conclusion: This study tends to confirm the possible impact of prenatal exposure to solvents on externalizing disorders, but this impact seems to be attenuated at age 6 compared to age 2. The association between internalizing disorders and prenatal exposure to solvents requires replication.

Maternal Exposure to Occupational Asthmagens During Pregnancy and Autism Spectrum Disorder in the Study to Explore Early Development.

Maternal immune activity has been linked to children with autism spectrum disorder (ASD). We examined maternal occupational exposure to asthma-causing agents during pregnancy in relation to ASD risk. Our sample included 463 ASD cases and 710 general population controls from the Study to Explore Early Development whose mothers reported at least one job during pregnancy. Asthmagen exposure was estimated from a published job-exposure matrix. The adjusted odds ratio for ASD comparing asthmagen-exposed to unexposed was 1.39 (95 % CI 0.96–2.02). Maternal workplace asthmagen exposure was not associated with ASD risk in this study, but this result does not exclude some involvement of maternal exposure to asthma-causing agents in ASD.Electronic supplementary materialThe online version of this article (doi:10.1007/s10803-016-2882-6) contains supplementary material, which is available to authorized users.