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Adverse childhood experiences (ACEs) have been associated with poor mental health outcomes in adulthood. Childhood maltreatment is related to both depressive and anxiety symptoms. Our objective was to investigate these associations among low-income, mostly Black and Latino men who have sex with men (MSM), as these may be a particularly vulnerable population group. Data come from a longitudinal study of MSM with varied substance use behaviors (n = 321) collected between August 2014 and April 2022. Cumulative, childhood maltreatment ACEs, and the single ACE of childhood sexual abuse were investigated as potential predictors of self-reported depressive and anxiety symptoms in mixed-effects logistic and ordinal regression models. There was no evidence of a dose-response relationship between the number of ACEs and the predicted probability of depressive and anxiety symptoms. Compared to MSM reporting fewer than five ACEs, those with five or more ACEs had approximately double the odds ratio of reporting depressive (OR = 1.93; 95% CI: 1.04-3.60) and anxiety symptoms (OR = 2.21; 95% CI: 1.05-4.68). The dimension of childhood maltreatment had a more robust prediction of depressive symptoms than the dimension of household dysfunction across all models. The association between childhood sexual abuse history and depressive symptoms remained after adjustment for the other nine ACEs (OR = 2.27; 95% CI: 1.11-4.68). The ordinal logistic model suggested that cumulative ACEs more than triple the odds of being in a higher anxiety category (OR = 3.12; 95% CI: 1.58-6.14), with associations reported for childhood maltreatment ACEs (OR = 1.31; 95% CI: 1.06-1.66) and childhood sexual abuse (OR = 1.93; 95% CI: 0.89-4.21). Childhood maltreatment ACEs, particularly childhood sexual abuse, are salient predictors of depressive and anxiety symptoms among adult urban MSM. Mitigating the impact of childhood maltreatment requires understanding the additional burden of social distress often faced by MSM throughout the life course.

BackgroundThis study examines how neighborhood socioeconomic status (nSES) and ethnic composition are associated with breast cancer risk for Asian American women.MethodsWe linked individual level data from a population-based case-control study of breast cancer among Asian American women with neighborhood level data in the Greater San Francisco Bay Area (cases: n = 118, controls: n = 390). Multivariable logistic regression models examined the association between nSES, ethnic composition, and odds of having breast cancer.ResultsAsian American women living in neighborhoods with high nSES and high ethnic composition had the highest odds of breast cancer, compared to those living in neighborhoods with high nSES and low ethnic composition (OR = 0.34, 95% CI [0.16-0.75]) or in neighborhoods with low nSES and high ethnic composition (OR = 0.37, 95% CI [0.17-0.83]).DiscussionNeighborhood socioeconomic and ethnic contexts are associated with breast cancer for Asian American women. We discuss explanations and avenues for future research.

Acetaminophen is the most common over-the-counter pain and fever medication used by pregnant women. While European studies suggest acetaminophen exposure in pregnancy could affect childhood asthma development, findings are less consistent in other populations. We evaluated whether maternal prenatal acetaminophen use is associated with childhood asthmatic symptoms (asthma diagnosis, wheeze, dry cough) in a Los Angeles cohort of 1201 singleton births. We estimated risk ratio (RR) and 95% confidence interval (CI) for childhood asthmatic outcomes according to prenatal acetaminophen exposure. Effect modification by maternal race/ethnicity and psychosocial stress during pregnancy was evaluated. The risks for asthma diagnosis (RR = 1.39, 95% CI 0.96, 2.00), wheezing (RR = 1.25, 95% CI 1.01, 1.54) and dry cough (RR =1.35, 95% CI 1.06, 1.73) were higher in children born to mothers who ever used acetaminophen during pregnancy compared with non-users. Black/African American and Asian/Pacific Islander children showed a greater than two-fold risk for asthma diagnosis and wheezing associated with the exposure. High maternal psychosocial stress also modified the exposure-outcome relationships. Acetaminophen exposure during pregnancy was associated with childhood asthmatic symptoms among vulnerable subgroups in this cohort. A larger study that assessed prenatal acetaminophen exposure with other social/environmental stressors and clinically confirmed outcomes is needed.

PurposeTo examine associations between parental occupation and childhood germ cell tumors (GCTs) in offspring while distinguishing by common histologic subtype (i.e., yolk sac tumor and teratoma).MethodsThis population-based case-control study included childhood GCT cases in Denmark diagnosed 1968-2015 (

BackgroundPreviously, numerous epidemiologic studies reported an association between autism spectrum disorder (ASD) and exposure to air pollution during pregnancy. However, there have been no metabolomics studies investigating the impact of pregnancy pollution exposure to ASD risk in offspring.ObjectivesTo identify differences in maternal metabolism that may reflect a biological response to exposure to high air pollution in pregnancies of offspring who later did or did not develop ASD.MethodsWe obtained stored mid-pregnancy serum from 214 mothers who lived in California's Central Valley and experienced the highest levels of air pollution during early pregnancy. We estimated each woman's average traffic-related air pollution exposure (carbon monoxide, nitric oxides, and particulate matter

ObjectiveTo examine associations with occupational livestock or other animal dust exposure and offspring cancer risk.MethodsIn this population-based case-control study of Danish children aged

BackgroundMaternal exposure to traffic-related air pollution during pregnancy has been shown to increase the risk of adverse birth outcomes and neurodevelopmental disorders. By utilizing high-resolution metabolomics (HRM), we investigated perturbations of the maternal serum metabolome in response to traffic-related air pollution to identify biological mechanisms.MethodsWe retrieved stored mid-pregnancy serum samples from 160 mothers who lived in the Central Valley of California known for high air particulate levels. We estimated prenatal traffic-related air pollution exposure (carbon monoxide, nitric oxides, and particulate matter

ObjectiveTo assess prenatal air toxics exposure and risk for childhood germ cell tumors (GCTs) by histological subtype (yolk sac tumor and teratoma).MethodsIn this case-control study, GCT cases less than 6 years (n = 243) identified from California Cancer Registry records were matched by birth year to cancer-free population controls (n = 147,100), 1984 to 2013. Routinely monitored air toxic exposures were linked to subjects' birth address. Logistic regression estimated GCT risks per interquartile range increase in exposure.ResultsPrenatal exposure to various highly-correlated, traffic-related air toxics during the second trimester increased GCT risk, particularly 1,3-butadiene (odds ratio [OR] = 1.51; 95% confidence interval [CI] = 1.01, 2.26) and meta/para-xylene (OR = 1.56; 95% CI = 1.10, 2.21). Analyses by subtype indicated elevated ORs for yolk sac tumors but not teratomas.ConclusionOur estimated ORs are consistent with positive associations between some prenatal traffic-related air toxics and GCT risk, notably yolk sac tumors.

IntroductionGiven rising rates of breast cancer in parts of Asia, immigrant Asian American women in the United States may have higher rates of breast cancer than previously anticipated. This study examined breast cancer risk among Asian American women by nativity and percentage of life lived in the United States, accounting for established breast cancer risk factors.MethodsWe analyzed a breast cancer case-control data set of Asian American women living in the San Francisco Bay Area; this data set included 132 cases of women with breast cancer selected from a Surveillance, Epidemiology, and End Results cancer registry and 438 Asian American women without diagnosed breast cancer matched to cases by age and country of origin. We used logistic regression to compare 3 Asian American groups: US-born, immigrants who lived 50% or more of their life in the United States, and immigrants who lived less than 50% of their life in the United States.ResultsIn the minimally adjusted and fully adjusted models, both groups of immigrant Asian American women had higher risk of breast cancer than US-born Asian American women. In the fully adjusted model, compared with US-born Asian American women, immigrant Asian American women who lived more than 50% of their life in United States were on average 3 times as likely (odds ratio = 3.00; 95% confidence interval, 1.56-5.75) and immigrants who lived less than 50% of their life in United States were on average 2.46 times as likely (odds ratio = 2.46; 95% confidence interval, 1.21-4.99) to have breast cancer. We found no difference in fully adjusted odds ratios of having breast cancer between the 2 immigrant groups.ConclusionThis study provides preliminary evidence that breast cancer risk among immigrant Asian American women may be higher than among their US-born counterparts.

ObjectivesWe examined associations between parental occupational chemical exposures up to 10 years before conception and the risk of sporadic retinoblastoma among offspring.MethodsIn our multicentre study on non-familial retinoblastoma, parents of 187 unilateral and 95 bilateral cases and 155 friend controls were interviewed by telephone. Exposure information was collected retroactively through a detailed occupational questionnaire that asked fathers to report every job held in the 10 years before conception, and mothers 1 month before and during the index pregnancy. An industrial hygienist reviewed all occupational data and assigned an overall exposure score to each job indicating the presence of nine hazardous agents.ResultsWe estimated elevated ORs for unilateral and bilateral retinoblastoma among offspring of fathers who were exposed to polycyclic aromatic hydrocarbons or paints in the 10 years before conception. However, only for exposure to paints did confidence limits exclude the null for bilateral disease (OR: 8.76, 95% CI: 1.32 to 58.09). Maternal prenatal exposure to at least one of the nine agents was related to increased risk of unilateral disease in their children (OR: 5.25, 95% CI: 1.14 to 24.16). Fathers exposed to at least one of the nine agents and who were ≥30 years of age were at increased risk of having a child diagnosed with bilateral retinoblastoma (OR: 6.59, 95% CI: 1.34 to 32.42).ConclusionsOur results suggest a role for several hazardous occupational exposures in the development of childhood retinoblastoma.

In a town located in a desert area of Northern Chile, gold and copper open-pit mining is carried out involving explosive processes. These processes are associated with increased dust exposure, which might affect children's respiratory health. Therefore, we aimed to quantify the causal attributable risk of living close to the mines on asthma or allergic rhinoconjunctivitis risk burden in children. Data on the prevalence of respiratory diseases and potential confounders were available from a cross-sectional survey carried out in 2009 among 288 (response: 69 % ) children living in the community. The proximity of the children's home addresses to the local gold and copper mine was calculated using geographical positioning systems. We applied targeted maximum likelihood estimation to obtain the causal attributable risk (CAR) for asthma, rhinoconjunctivitis and both outcomes combined. Children living more than the first quartile away from the mines were used as the unexposed group. Based on the estimated CAR, a hypothetical intervention in which all children lived at least one quartile away from the copper mine would decrease the risk of rhinoconjunctivitis by 4.7 percentage points (CAR: - 4.7 ; 95 % confidence interval ( 95 % CI): - 8.4 ; - 0.11 ); and 4.2 percentage points (CAR: - 4.2 ; 95 % CI: - 7.9 ; - 0.05 ) for both outcomes combined. Overall, our results suggest that a hypothetical intervention intended to increase the distance between the place of residence of the highest exposed children would reduce the prevalence of respiratory disease in the community by around four percentage points. This approach could help local policymakers in the development of efficient public health strategies.

In a town located in a desert area of Northern Chile, gold and copper open-pit mining is carried out involving explosive processes. These processes are associated with increased dust exposure, which might affect children's respiratory health. Therefore, we aimed to quantify the causal attributable risk of living close to the mines on asthma or allergic rhinoconjunctivitis risk burden in children. Data on the prevalence of respiratory diseases and potential confounders were available from a cross-sectional survey carried out in 2009 among 288 (response: 69 % ) children living in the community. The proximity of the children's home addresses to the local gold and copper mine was calculated using geographical positioning systems. We applied targeted maximum likelihood estimation to obtain the causal attributable risk (CAR) for asthma, rhinoconjunctivitis and both outcomes combined. Children living more than the first quartile away from the mines were used as the unexposed group. Based on the estimated CAR, a hypothetical intervention in which all children lived at least one quartile away from the copper mine would decrease the risk of rhinoconjunctivitis by 4.7 percentage points (CAR: - 4.7 ; 95 % confidence interval ( 95 % CI): - 8.4 ; - 0.11 ); and 4.2 percentage points (CAR: - 4.2 ; 95 % CI: - 7.9 ; - 0.05 ) for both outcomes combined. Overall, our results suggest that a hypothetical intervention intended to increase the distance between the place of residence of the highest exposed children would reduce the prevalence of respiratory disease in the community by around four percentage points. This approach could help local policymakers in the development of efficient public health strategies.

ObjectivesAdverse childhood experiences (ACEs) have been linked to a variety of diseases in adulthood, including cancer. However, current research has yet to determine if all abuse types are associated with cancer and if women are more adversely impacted by ACEs than men.MethodsData from the 2011 Behavioral Risk Factor Surveillance System, a national survey of American adults 18 and older (N = 111,964) were analyzed. Logistic regression models were fit to estimate odds of ever being diagnosed with cancer after experiencing one or more of eight different ACEs, while adjusting for potential confounders. These analyses were then stratified by gender.ResultsAmong women, childhood experiences of physical abuse, sexual abuse, emotional abuse, living with someone who was mentally ill, living with a problem drinker, living with a drug user, and living in a household where adults treated each other violently were associated with higher odds of cancer. Among men, only emotional abuse was associated with higher odds of cancer.ConclusionsResults suggest that ACEs increase risk of cancer later in life. However, this impact occurs mostly among women. This finding may be because women experience many ACEs at higher rates than men and because women, via sexual abuse, can be exposed to cancer-causing viruses.

PurposeTo examine whether parental pesticide exposure contributes to the development of sporadic retinoblastoma.DesignCase-control study.MethodsData were collected by a large multicenter study of sporadic retinoblastoma in which parents of 99 unilateral and 56 bilateral age-matched case-control pairs were interviewed by telephone. Retrospective exposure information was collected on the type, location, timing, and frequency of residential pesticide use. We used conditional logistic regression analyses to estimate odds ratios for maternal pesticide exposure in the month before or during pregnancy and to assess whether the type of product, and the circumstances under which it was applied, were associated with risk of disease.ResultsUnilateral retinoblastoma was associated with parental insecticide use (odds ratio [OR], 2.8; confidence interval [CI], 1.1-6.7) and the use of professional lawn or landscape services (OR, 2.8; CI, 1.0-8.2). For bilateral disease we observed large point estimates for several exposures but the small number of cases rendered these results uninformative (ie, resulted in wide confidence intervals). Whether parents used the pesticide inside vs outside the home did not appear to modify risk estimates for unilateral retinoblastoma (OR, 2.5; CI, 0.9-7.0 vs OR, 2.5; CI, 1.0-6.5), nor did the type, frequency, timing related to pregnancy, or applicator of pesticide used influence estimates to an appreciable degree for disease.ConclusionsOur results suggest that parental pesticide exposure before or during pregnancy may play a role in the development of childhood retinoblastoma. Retrospectively collected exposure data introduces the possibility of recall bias; therefore, results should be interpreted cautiously until additional studies are conducted.

Adverse childhood experiences (ACEs) have been linked to increased use of tobacco products later in life. However, studies to date have ignored smokeless tobacco products. To address this, data from the 2011 Behavioral Risk Factor Surveillance System, which interviewed adults 18 years and over (N = 102,716) were analyzed. Logistic regression models were fit to estimate odds ratios of ever smoking, current smoking and current smokeless tobacco use in relation to ACEs. Results showed that less than 4 % of respondents currently used smokeless tobacco products, while 44.95 and 18.57 % reported ever and current smoking, respectively. Physical abuse (OR 1.40; 95 % CI 1.14, 1.72), emotional abuse (OR 1.41; 95 % CI 1.19, 1.67), sexual abuse (OR 0.70; 95 % CI 0.51, 0.95), living with a drug user (OR 1.50; 95 % CI 1.17, 1.93), living with someone who was jailed (OR 1.50; 95 % CI 1.11, 2.02) and having parents who were separated or divorced (OR 1.31; 95 % CI 1.09, 1.57) were associated with smokeless tobacco use in unadjusted models. After accounting for confounders, physical abuse (OR 1.43; 95 % CI 1.16, 1.78), emotional abuse (OR 1.32; 95 % CI 1.10, 1.57), living with a problem drinker (OR 1.30; 95 % CI 1.08, 1.58), living with a drug user (OR 1.31; 95 % CI 1.00, 1.72) and living with adults who treated each other violently (OR 1.30; 95 % CI 1.05, 1.62) were associated with smokeless tobacco use. Living with someone who was mentally ill (OR 0.70; 95 % CI 0.53, 0.92) was associated with smokeless tobacco use after accounting for confounders and all ACEs. Results indicated that some childhood adversities are associated with use of smokeless tobacco products. Special attention is needed to prevent tobacco use of different types among those experiencing ACEs.

Prenatal psychosocial stressors may increase the risk of wheeze in young offspring, yet little attention has been given to the effects that maternal ethnicity may have on this relationship. From a population-based cohort of 1193 children, we assessed the effect of maternal prenatal stressors on the risk of lifetime wheeze in young offspring. We further studied whether maternal Latina ethnicity modified these associations. The risk of wheeze in the offspring was increased from high levels of pregnancy anxiety (aRR 1.40, 95 % CI 1.07, 1.83), negative life events (aRR 1.36, 95 % CI 1.06, 1.75), or low paternal support (aRR 1.41, 95 % CI 1.02, 1.96). The risk of lifetime wheeze was stronger in the offspring of Latina mothers than of White mothers for these same stressors. Multiple maternal prenatal stressors are associated with increased risk of lifetime wheeze in young offspring, with slight effect modification by Latina ethnicity.

Research on synergism of stress and air pollution on adolescent lung function is uncommon. Our study found statistically significant synergism between select psychosocial stressors and air pollution on the lung function of adolescents.

BackgroundLittle is known about the influence of environmental factors on the etiology of childhood brain tumors.ObjectivesWe examined risks for brain tumors in children after prenatal and infant exposure to monitored ambient air toxics.MethodsWe ascertained all cases of medulloblastoma, central nervous system primitive neuroectodermal tumor (PNET), and astrocytoma before 6 years of age diagnosed in 1990-2007 from the California Cancer Registry and selected controls randomly from birth rolls matched by birth year. Exposures to air toxics during pregnancy/infancy for 43 PNET, 34 medulloblastoma, and 106 astrocytoma cases and 30,569 controls living within 5 mi of a monitor were determined. With factor analysis we assessed the correlational structures of 26 probable carcinogenic toxics, and estimated odds ratios by brain tumor type in logistic regression models.ResultsPNETs (≤ 38 cases) were positively associated with interquartile range (IQR) increases in prenatal exposure to acetaldehyde [odds ratio (OR) = 2.30; 95% CI: 1.44, 3.67], 1,3-butadiene (OR = 2.23; 95% CI: 1.28, 3.88), benzene, and toluene; and with IQR increases in exposure during the first year of life to ortho-dichlorobenzene (OR = 3.27; 95% CI: 1.17, 9.14), 1,3-butadiene (OR = 3.15; 95% CI: 1.57, 6.32), and benzene. All exposures except ortho-dichlorobenzene loaded on the same factor. Medulloblastoma (≤ 30 cases) was associated with prenatal exposure to polycyclic aromatic hydrocarbons (PAHs combined: OR = 1.44; 95% CI: 1.15, 1.80). Exposures to lead and some PAHs during the first year of life were positively associated with astrocytoma, but the confidence intervals included the null value (e.g., for lead, OR = 1.40; 95% CI: 0.97, 2.03).ConclusionsOur data suggest that in utero and infancy exposures to air toxics generated by industrial and road traffic sources may increase the risk of PNET and medulloblastoma, with limited support for increased risks for astrocytoma in children up to age 6.Citationvon Ehrenstein OS, Heck JE, Park AS, Cockburn M, Escobedo L, Ritz B. 2016. In Utero and early-life exposure to ambient air toxics and childhood brain tumors: a population-based case-control study in California, USA. Environ Health Perspect 124:1093-1099; http://dx.doi.org/10.1289/ehp.1408582.

Previous research has generally found exclusive breastfeeding to protect against asthma in young children. However, maternal nativity in a Latina population has not been assessed as a potential confounder or effect modifier. Using cross-sectional data restricted to Latina mothers (n = 704) from a birth cohort in Los Angeles interviewed in 2003 and 2006, we estimated risk ratios (RR) for exclusive breastfeeding and asthmatic symptoms in the offspring. 56 children (8%) had asthmatic symptoms at age 3.5 years. We found a 49% reduction in risk of asthmatic symptoms with >3 months of exclusive breastfeeding (aRR 0.51, 95% CI 0.28, 0.90). Foreign-born Latinas were more likely to initiate and continue breastfeeding for at least 3 months compared with US-born Latinas. Three or more months of exclusive breastfeeding reduced the risk of asthmatic symptoms in the offspring of Latinas, and maternal nativity did not confound or modify this association.

BackgroundThe early age at retinoblastoma occurrence, the most common eye malignancy in childhood, suggests that perinatal factors may contribute to its etiology.MethodsIn a large multicenter study of non-familial retinoblastoma, we conducted structured interviews with the parents of 280 cases and 146 controls to elicit information on health during the perinatal period. We used unconditional logistic regression to assess associations between retinoblastoma and parental fertility treatment, birth control use in the year prior to pregnancy, maternal health conditions and the use of prescription medications during pregnancy, and whether mothers breastfed the index child.ResultsBilateral retinoblastoma was related to maternal underweight (body mass index

Phenols and parabens show some evidence for endocrine disruption in laboratory animals. The goal of the Methods Advancement for Milk Analysis (MAMA) Study was to develop or adapt methods to measure parabens (methyl, ethyl, butyl, propyl) and phenols (bisphenol A (BPA), 2,4- and 2,5-dichlorophenol, benzophenone-3, triclosan) in urine, milk and serum twice during lactation, to compare concentrations across matrices and with endogenous biomarkers among 34 North Carolina women. These non-persistent chemicals were detected in most urine samples (53-100%) and less frequently in milk or serum; concentrations differed by matrix. Although urinary parabens, triclosan and dichlorophenols concentrations correlated significantly at two time points, those of BPA and benzophenone-3 did not, suggesting considerable variability in those exposures. These pilot data suggest that nursing mothers are exposed to phenols and parabens; urine is the best measurement matrix; and correlations between chemical and endogenous immune-related biomarkers merit further investigation.

BackgroundPerfluoroalkyl substances (PFASs) are persistent pollutants found to be endocrine disruptive and neurotoxic in animals. Positive correlations between PFASs and neurobehavioral problems in children were reported in cross-sectional data, but findings from prospective studies are limited.ObjectivesWe investigated whether prenatal exposure to PFASs is associated with attention deficit/hyperactivity disorder (ADHD) or childhood autism in children.MethodsAmong 83,389 mother-child pairs enrolled in the Danish National Birth Cohort during 1996-2002, we identified 890 ADHD cases and 301 childhood autism cases from the Danish National Hospital Registry and the Danish Psychiatric Central Registry. From this cohort, we randomly selected 220 cases each of ADHD and autism, and we also randomly selected 550 controls frequency matched by child's sex. Sixteen PFASs were measured in maternal plasma collected in early or mid-pregnancy. We calculated risk ratios (RRs) using generalized linear models, taking into account sampling weights.ResultsPerfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were detected in all samples; four other PFASs were quantified in ≥ 90% of the samples. We did not find consistent evidence of associations between mother's PFAS plasma levels and ADHD [per natural log nanograms per milliliter increase: PFOS RR = 0.87 (95% CI: 0.74, 1.02); PFOA RR = 0.98 (95% CI: 0.82, 1.16)] or autism [per natural log nanograms per milliliter increase: PFOS RR = 0.92 (95% CI: 0.69, 1.22); PFOA RR = 0.98 (95% CI: 0.73, 1.31)]. We found positive as well as negative associations between higher PFAS quartiles and ADHD in models that simultaneously adjusted for all PFASs, but these estimates were imprecise.ConclusionsIn this study we found no consistent evidence to suggest that prenatal PFAS exposure increases the risk of ADHD or childhood autism in children.

BackgroundGenetic and environmental factors are believed to contribute to the development of autism, but relatively few studies have considered potential environmental risks. Here, we examine risks for autism in children related to in utero exposure to monitored ambient air toxics from urban emissions.MethodsAmong the cohort of children born in Los Angeles County, California, 1995-2006, those whose mothers resided during pregnancy in a 5-km buffer around air toxics monitoring stations were included (n = 148,722). To identify autism cases in this cohort, birth records were linked to records of children diagnosed with primary autistic disorder at the California Department of Developmental Services between 1998 and 2009 (n = 768). We calculated monthly average exposures during pregnancy for 24 air toxics selected based on suspected or known neurotoxicity or neurodevelopmental toxicity. Factor analysis helped us identify the correlational structure among air toxics, and we estimated odds ratios (ORs) for autism from logistic regression analyses.ResultsAutism risks were increased per interquartile range increase in average concentrations during pregnancy of several correlated toxics mostly loading on 1 factor, including 1,3-butadiene (OR = 1.59 [95% confidence interval = 1.18-2.15]), meta/para-xylene (1.51 [1.26-1.82]), other aromatic solvents, lead (1.49 [1.23-1.81]), perchloroethylene (1.40 [1.09-1.80]), and formaldehyde (1.34 [1.17-1.52]), adjusting for maternal age, race/ethnicity, nativity, education, insurance type, parity, child sex, and birth year.ConclusionsRisks for autism in children may increase following in utero exposure to ambient air toxics from urban traffic and industry emissions, as measured by community-based air-monitoring stations.

OBJECTIVE: Our understanding of the influence of maternal race/ethnicity and nativity and childhood autistic disorder (AD) in African Americans/blacks, Asians, and Hispanics in the United States is limited. Phenotypic differences in the presentation of childhood AD in minority groups may indicate etiologic heterogeneity or different thresholds for diagnosis. We investigated whether the risk of developing AD and AD phenotypes differed according to maternal race/ethnicity and nativity. METHODS: Children born in Los Angeles County with a primary AD diagnosis at ages 3 to 5 years during 1998-2009 were identified and linked to 1995-2006 California birth certificates (7540 children with AD from a cohort of 1,626,354 births). We identified a subgroup of children with AD and a secondary diagnosis of mental retardation and investigated heterogeneity in language and behavior. RESULTS: We found increased risks of being diagnosed with AD overall and specifically with comorbid mental retardation in children of foreign-born mothers who were black, Central/South American, Filipino, and Vietnamese, as well as among US-born Hispanic and African American/black mothers, compared with US-born whites. Children of US African American/black and foreign-born black, foreign-born Central/South American, and US-born Hispanic mothers were at higher risk of exhibiting an AD phenotype with both severe emotional outbursts and impaired expressive language than children of US-born whites. CONCLUSIONS: Maternal race/ethnicity and nativity are associated with offsprings AD diagnosis and severity. Future studies need to examine factors related to nativity and migration that may play a role in the etiology as well as identification and diagnosis of AD in children.

ObjectivesFocusing on Latinas, we investigated whether maternal occupations during pregnancy increase term low birth weight (TLBW) (less than 2500 g; 37 weeks or more).MethodsIn a case-control study (n = 1498) nested within a 2003 birth cohort (n = 58,316) in Los Angeles County, California (65% Latina), we assessed the influence of maternal occupation on TLBW, using Occupational Codes based on the 2000 US Census Occupational Classification System.ResultsOdds ratios (ORs) for TLBW were increased among women working during pregnancy in "transportation and material moving operations" (adjusted OR = 3.28; 95% confidence interval = 1.00 to 10.73), "food preparation and serving occupations" (adjusted OR = 3.03, 95% confidence interval = 1.21 to 7.62), or "production occupations" (adjusted OR = 2.63, 95% confidence interval = 1.01 to 6.82) compared with "office occupations;" 73% to 93% of women working in these higher-risk jobs were immigrant Latinas.ConclusionsWorking conditions in various jobs held mainly by first-generation immigrant Latinas increase risks for TLBW and need to be addressed to develop strategies to reduce TLBW.

BackgroundArsenic exposure via drinking water increases the risk of chronic respiratory disease in adults. However, information on pulmonary health effects in children after early life exposure is limited.MethodsThis population-based cohort study set in rural Matlab, Bangladesh, assessed lung function and respiratory symptoms of 650 children aged 7-17 years. Children with in utero and early life arsenic exposure were compared with children exposed to less than 10 µg/l in utero and throughout childhood. Because most children drank the same water as their mother had drunk during pregnancy, we could not assess only in utero or only childhood exposure.ResultsChildren exposed in utero to more than 500 µg/l of arsenic were more than eight times more likely to report wheezing when not having a cold [odds ratio (OR) = 8.41, 95% confidence interval (CI): 1.66-42.6, P < 0.01] and more than three times more likely to report shortness of breath when walking on level ground (OR = 3.86, 95% CI: 1.09-13.7, P = 0.02) and when walking fast or climbing (OR = 3.19, 95% CI: 1.22-8.32, P < 0.01]. However, there was little evidence of reduced lung function in either exposure category.ConclusionsChildren with high in utero and early life arsenic exposure had marked increases in several chronic respiratory symptoms, which could be due to in utero exposure or to early life exposure, or to both. Our findings suggest that arsenic in water has early pulmonary effects and that respiratory symptoms are a better marker of early life arsenic toxicity than changes in lung function measured by spirometry.

BackgroundIngested inorganic arsenic (InAs) is methylated to monomethylated (MMA) and dimethylated metabolites (DMA). Methylation may have an important role in arsenic toxicity, because the monomethylated trivalent metabolite [MMA(III)] is highly toxic.ObjectivesWe assessed the relationship of creatinine and nutrition--using dietary intake and blood concentrations of micronutrients--with arsenic metabolism, as reflected in the proportions of InAS, MMA, and DMA in urine, in the first study that incorporated both dietary and micronutrient data.MethodsWe studied methylation patterns and nutritional factors in 405 persons who were selected from a cross-sectional survey of 7,638 people in an arsenic-exposed population in West Bengal, India. We assessed associations of urine creatinine and nutritional factors (19 dietary intake variables and 16 blood micronutrients) with arsenic metabolites in urine.ResultsUrinary creatinine had the strongest relationship with overall arsenic methylation to DMA. Those with the highest urinary creatinine concentrations had 7.2% more arsenic as DMA compared with those with low creatinine (p < 0.001). Animal fat intake had the strongest relationship with MMA% (highest tertile animal fat intake had 2.3% more arsenic as MMA, p < 0.001). Low serum selenium and low folate were also associated with increased MMA%.ConclusionsUrine creatinine concentration was the strongest biological marker of arsenic methylation efficiency, and therefore should not be used to adjust for urine concentration in arsenic studies. The new finding that animal fat intake has a positive relationship with MMA% warrants further assessment in other studies. Increased MMA% was also associated, to a lesser extent, with low serum selenium and folate.

This study was conducted to monitor the changes in arsenic concentration during different seasons in a one-year period during 2002-2003 in selected tubewells in an arsenic-affected area in the district of South 24 Parganas in West Bengal, India, and to map the location of the wells. Seasonal variations in concentrations of arsenic in water were measured from 74 selected tubewells, ranging in depth from 40 to 500 feet. Water samples were collected from these wells during winter, summer, monsoon, and the following winter in 2002-2003. A global positioning system was used for locating the tubewells, and a geographic information system was used for mapping. There was evidence of seasonal variation in concentrations of arsenic in water (p=0.02) with the minimum average concentration occurring in the summer season (694 microg/L) and the maximum in the monsoon season (906 microg/L). From the winter of 2002 to the winter of 2003, arsenic concentrations increased, irrespective of the depth of the tubewells, from an average of 464 microg/L to 820 microg/L (p

Arsenic in drinking water is an established cause of lung cancer, and preliminary evidence suggests that ingested arsenic may also cause nonmalignant lung disease. Antofagasta is the second largest city in Chile and had a distinct period of very high arsenic exposure that began in 1958 and lasted until 1971, when an arsenic removal plant was installed. This unique exposure scenario provides a rare opportunity to investigate the long-term mortality impact of early-life arsenic exposure. In this study, we compared mortality rates in Antofagasta in the period 1989-2000 with those of the rest of Chile, focusing on subjects who were born during or just before the peak exposure period and who were 30-49 years of age at the time of death. For the birth cohort born just before the high-exposure period (1950-1957) and exposed in early childhood, the standardized mortality ratio (SMR) for lung cancer was 7.0 [95% confidence interval (CI), 5.4-8.9; p

There has been widespread speculation about whether nutritional deficiencies increase the susceptibility to arsenic health effects. This is the first study to investigate whether dietary micronutrient and macronutrient intake modulates the well-established human risk of arsenic-induced skin lesions, including alterations in skin pigmentation and keratoses. The study was conducted in West Bengal, India, which along with Bangladesh constitutes the largest population in the world exposed to arsenic from drinking water. In this case-control study design, cases were patients with arsenic-induced skin lesions and had < 500 microg/L arsenic in their drinking water. For each case, an age- and sex-matched control was selected from participants of a 1995-1996 cross-sectional survey, whose drinking water at that time also contained < 500 microg/L arsenic. Nutritional assessment was based on a 24-hr recall for major dietary constituents and a 1-week recall for less common constituents. Modest increases in risk were related to being in the lowest quintiles of intake of animal protein [odds ratio (OR) = 1.94; 95% confidence interval (CI), 1.05-3.59], calcium (OR = 1.89; 95% CI, 1.04-3.43), fiber (OR = 2.20; 95% CI, 1.15-4.21), and folate (OR = 1.67; 95% CI, 0.87-3.2). Conditional logistic regression suggested that the strongest associations were with low calcium, low animal protein, low folate, and low fiber intake. Nutrient intake was not related to arsenic exposure. We conclude that low intake of calcium, animal protein, folate, and fiber may increase susceptibility to arsenic-caused skin lesions. However, in light of the small magnitude of increased risks related to these dietary deficiencies, prevention should focus on reducing exposure to arsenic.