Maternal acetaminophen use during pregnancy is associated with a higher risk for HKDs and ADHD-like behaviors in children. Because the exposure and outcome are frequent, these results are of public health relevance but further investigations are needed.

NCT01564992.

Despite numerous studies of air pollution and adverse birth outcomes, few studies have investigated preeclampsia and gestational hypertension, two pregnancy disorders with serious consequences for both mother and infant. Relying on hospital birth records, we conducted a cohort study identifying 34,705 singleton births delivered at Magee-Women’s Hospital in Pittsburgh, PA between 1997 and 2002. Particle (<10 μm-PM10; <2.5 μm-PM2.5) and ozone (O3) exposure concentrations in the first trimester of pregnancy were estimated using the space–time ordinary Kriging interpolation method. We employed multiple logistic regression estimate associations between first trimester exposures and preeclampsia, gestational hypertension, preterm delivery, and small for gestational age (SGA) infants. PM2.5 and O3 exposures were associated with preeclampsia (adjusted OR = 1.15, 95 % CI = 0.96–1.39 per 4.0 μg/m3 increase in PM2.5; adjusted OR = 1.12, 95 % CI = 0.89–1.42 per 16.8 ppb increase in O3), gestational hypertension (for PM2.5 OR = 1.11, 95 % CI = 1.00–1.23; for O3 OR = 1.12, 95 % CI = 0.97–1.29), and preterm delivery (for PM2.5 ORs = 1.10, 95 % CI = 1.01–1.20; for O3 ORs = 1.23, 95 % CI = 1.01–1.50). Smaller 5–8 % increases in risk were also observed for PM10 with gestational hypertension and SGA, but not preeclampsia. Our data suggest that first trimester exposure to particles, mostly PM2.5, and ozone, may increase the risk of developing preeclampsia and gestational hypertension, as well as preterm delivery and SGA.

BackgroundVery little is currently known about air pollutants’ adverse effects on neurodegenerative diseases even though recent studies have linked particulate exposures to brain pathologies associated with Parkinson’s and Alzheimer’s disease.ObjectiveIn the present study, we investigated long-term exposure to traffic-related air pollution and Parkinson’s disease.MethodsIn a case–control study of 1,696 Parkinson’s disease (PD) patients identified from Danish hospital registries and diagnosed 1996–2009 and 1,800 population controls matched by sex and year of birth, we assessed long-term traffic-related air pollutant exposures (represented by nitrogen dioxide; NO2) from a dispersion model, using residential addresses from 1971 to the date of diagnosis or first cardinal symptom for cases and the corresponding index date for their matched controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated with logistic regression, adjusting for matching factors and potential confounders.ResultsWe found ambient air pollution from traffic sources to be associated with risk of PD, with a 9% higher risk (95% CI: 3, 16.0%) per interquartile range increase (2.97 μg/m3) in modeled NO2. For participants living for ≥ 20 years in the capital city, ORs were larger (OR = 1.21; 95% CI: 1.11, 1.31) than in provincial towns (OR = 1.10; 95% CI: 0.97, 1.26), whereas there was no association among rural residents.ConclusionsOur findings raise concerns about potential effects of air pollution from traffic and other sources on the risk of PD, particularly in populations with high or increasing exposures.CitationRitz B, Lee PC, Hansen J, Funch Lassen C, Ketzel M, Sørensen M, Raaschou-Nielsen O. 2016. Traffic-related air pollution and Parkinson’s disease in Denmark: a case–control study. Environ Health Perspect 124:351–356; http://dx.doi.org/10.1289/ehp.1409313

Background It is not well understood how air pollution leads to adverse pregnancy outcomes. One pathway may be through C-reactive protein, a biomarker of systemic inflammation that has been reported to increase the risk of preterm delivery. We examined whether air pollution influences serum concentrations of C-reactive protein in early pregnancy. Methods We studied 1696 pregnant women in Allegheny County, PA, from 1997 through 2001. C-reactive protein concentrations were assayed in blood collected before the 22nd week of gestation. We estimated levels of particles of less than 10 μm (PM10) and less than 2.5 μm diameter (PM2.5), carbon monoxide, nitrogen dioxide, sulfur dioxide, and ozone at the maternal zip code using Kriging interpolation for measurements obtained from ambient stations. Associations between air pollution and high C-reactive protein concentrations (≥8 ng/mL) were evaluated using logistic regression. Results Among nonsmokers, an observed 9.2 μg/m3 increase in PM10 (averaged over 28 days prior to the blood sample) was associated with an odds ratios of 1.41 for high C-reactive protein concentrations (95% confidence interval = 0.99–2.00). Similarly, a 4.6 μg/m3 increase in PM2.5 was associated with an odds ratio of 1.47 (1.05–2.06). The odds ratio was 1.49 (0.75–2.96) per 7.9 ppb increase in ozone during summer. There were no associations in smokers or for other air pollutants, and there was no evidence for effect-measure modification by obesity. Conclusions PM10, PM2.5, and ozone exposures were associated with increased C-reactive protein concentrations in early pregnancy, suggesting that these air pollutants contribute to inflammation and thereby possibly to adverse pregnancy outcomes.

Objective: To assess whether being able to quit smoking is an early marker of Parkinson disease (PD) onset rather than tobacco being "neuroprotective," we analyzed information about ease of quitting and nicotine substitute use.Methods: For this case-control study, we identified 1,808 patients with PD diagnosed between 1996 and 2009 from Danish registries, matched 1,876 population controls on sex and year of birth, and collected lifestyle information. We estimated odds ratios and 95% confidence intervals with logistic regression adjusting for matching factors and confounders.Results: Fewer patients with PD than controls ever established a smoking habit. Among former smokers, those with greater difficulty quitting or using nicotine substitutes were less likely to develop PD, with the risk being lowest among those reporting "extremely difficult to quit" compared with "easy to quit." Nicotine substitute usage was strongly associated with quitting difficulty and duration of smoking, i.e., most strongly among current smokers, followed by former smokers who had used nicotine substitutes, and less strongly among former smokers who never used substitutes.Conclusions: Our data support the notion that patients with PD are able to quit smoking more easily than controls. These findings are compatible with a decreased responsiveness to nicotine during the prodromal phase of PD. We propose that ease of smoking cessation is an aspect of premanifest PD similar to olfactory dysfunction, REM sleep disorders, or constipation and suggests that the apparent "neuroprotective" effect of smoking observed in epidemiologic studies is due to reverse causation. Neurology ® 2014;83:1396-1402 GLOSSARY CI 5 confidence interval; GWAS 5 genome-wide association study; OR 5 odds ratio; PD 5 Parkinson disease.According to epidemiologic studies, patients with Parkinson disease (PD) are less likely to smoke.1-3 Also, those who smoke for longer are at lower risk while lengthening time since quitting increases PD risk, causing some to argue that smoking may protect against PD and even prompting nicotine PD prevention trials. 4 While this is counterintuitive given the otherwise adverse health effects of smoking, common biases including confounding, selection, or measurement error do not explain this finding. Alternatively, the possibility exists that biological mechanisms responsible for PD result in smoking avoidance or the ability to quit smoking more easily among those at risk of developing PD. That is, individuals who develop PD may not experience the positive reinforcement from, and possibly the addictive response to, nicotine many years before motor symptom development, and thus are able to quit more easily than smokers who never develop PD. This distinction is important because smoking may either provide leads for treatment/prevention of PD or be plainly no more than an early marker of insidious PD onset. To explore this, we examined difficulty quitting and use of nicotine substitutes in relation to PD risk in the Danish PASIDA (Parkinson...

Objectives: Traumatic brain injury (TBI) increased risk of Parkinson disease (PD) in many but not all epidemiologic studies, giving rise to speculations about modifying factors. A recent animal study suggested that the combination of TBI with subthreshold paraquat exposure increases dopaminergic neurodegeneration. The objective of our study was to investigate PD risk due to both TBI and paraquat exposure in humans.Methods: From 2001 to 2011, we enrolled 357 incident idiopathic PD cases and 754 population controls in central California. Study participants were asked to report all head injuries with loss of consciousness for .5 minutes. Paraquat exposure was assessed via a validated geographic information system (GIS) based on records of pesticide applications to agricultural crops in California since 1974. This GIS tool assesses ambient pesticide exposure within 500 m of residences and workplaces.Results: In logistic regression analyses, we observed a 2-fold increase in risk of PD for subjects who reported a TBI (adjusted odds ratio [AOR] 2.00, 95% confidence interval [CI] 1.28-3.14) and a weaker association for paraquat exposures (AOR 1.36, 95% CI 1.02-1.81). However, the risk of developing PD was 3-fold higher (AOR 3.01, 95% CI 1.51-6.01) in study participants with a TBI and exposure to paraquat than those exposed to neither risk factor.Conclusions: While TBI and paraquat exposure each increase the risk of PD moderately, exposure to both factors almost tripled PD risk. These environmental factors seem to act together to increase PD risk in a more than additive manner. Neurology Parkinson disease (PD), the second most common neurodegenerative disorder affecting 1%-2% of the population over 65 years of age, is characterized by progressive loss of dopamine neurons in substantia nigra pars compacta, leading to bradykinesia, rigidity, postural instability, and resting tremor as the cardinal motor features. It is widely acknowledged that PD etiology is most likely multifactorial. Lifestyle habits such as smoking and caffeine intake, genetic polymorphisms, environmental exposures to pesticides or metals, long-term exposure to certain medications, and interactions between these factors collectively appear to contribute to disease development. We have previously reported 2-to 3-fold increases in risk of developing PD when exposed to specific types or classes of pesticides, especially for combined exposures to paraquat and maneb, and for patients who carry genetic polymorphisms in susceptibility genes. 1,2 In the past 20 years, many but not all studies of traumatic brain injury (TBI) have linked head injuries with or without loss of consciousness to PD. [3][4][5][6][7][8][9][10] We speculated that TBI may require additional risk or susceptibility factors in order to cause PD, which has sometimes been referred

The majority of studies on parent-child discrepancies in the assessment of adolescent emotional and behavioral problems have been conducted in Western countries. It is believed that parent-adolescent agreement would be higher in societies with a strong culture of familism. We examined whether parent-adolescent discrepancies in the rating of adolescent emotional and behavioral problems are related to parental and family factors in Taiwan. Participants included 1,421 child-parent pairs of 7th-grade students from 12 middle schools in Northern Taiwan and their parents. We calculated Pearson’s correlation coefficients to assess the relationship between parental (Child Behavior Checklist, CBCL) and adolescent (Youth Self Report, YSR) report of emotional/behavioral problem syndromes. Regression models were used to assess parent-adolescent differences in relation to parental psychopathology and family factors. We found that parent-adolescent agreement was moderate (r = 0.37). Adolescents reported higher symptom scores than their parents (Mean Total Problem Score: CBCL: 20.79, YSR: 33.14). Parental psychopathology was related to higher parental ratings and better informant agreement. Parents with higher socioeconomic status (SES) tended to report lower scores for adolescent problem syndromes, resulting in higher levels of disagreement. Greater maternal care was related to higher parent-adolescent agreement. Based on our study findings, we conclude that familism values do not seem to improve parent-child agreement in the assessment of adolescent problem syndromes. The finding that higher SES was related to increased discrepancies speaks to the need to explore the culture-specific mechanisms giving rise to informant discrepancies.