Estimates of the prevalence of Parkinson’s disease in North America have varied widely and many estimates are based on small numbers of cases and from small regional subpopulations. We sought to estimate the prevalence of Parkinson’s disease in North America by combining data from a multi-study sampling strategy in diverse geographic regions and/or data sources. Five separate cohort studies in California (2), Minnesota (1), Hawaii USA (1), and Ontario, Canada (1) estimated the prevalence of PD from health-care records (3), active ascertainment through facilities, large group, and neurology practices (1), and longitudinal follow-up of a population cohort (1). US Medicare program data provided complementary estimates for the corresponding regions. Using our age- and sex-specific meta-estimates from California, Minnesota, and Ontario and the US population structure from 2010, we estimate the overall prevalence of PD among those aged ≥45 years to be 572 per 100,000 (95% confidence interval 537–614) that there were 680,000 individuals in the US aged ≥45 years with PD in 2010 and that that number will rise to approximately 930,000 in 2020 and 1,238,000 in 2030 based on the US Census Bureau population projections. Regional variations in prevalence were also observed in both the project results and the Medicare-based calculations with which they were compared. The estimates generated by the Hawaiian study were lower across age categories. These estimates can guide health-care planning but should be considered minimum estimates. Some heterogeneity exists that remains to be understood.

We evaluated the effect of air pollution exposure during pregnancy on the occurrence of preterm birth in a cohort of 97,518 neonates born in Southern California. We used measurements of carbon monoxide (CO), nitrogen dioxide, ozone, and particulate matter less than 10 microm (PM10) collected at 17 air-quality-monitoring stations to create average exposure estimates for periods of pregnancy. We calculated crude and adjusted risk ratios (RRs) for premature birth by period-specific ambient pollution levels. We observed a 20% increase in preterm birth per 50-microg increase in ambient PM10 levels averaged over 6 weeks before birth [RRcrude = 1.20; 95% confidence interval (CI) = 1.09-1.33] and a 16% increase when averaging over the first month of pregnancy (RRcrude = 1.16; 95% CI = 1.06-1.26). PM10 effects showed no regional pattern. CO exposure 6 weeks before birth consistently exhibited an effect only for the inland regions (RRcrude = 1.13; 95% CI = 1.08-1.18 per 3 parts per million), and during the first month of pregnancy, the effect was weak for all stations (RRcrude = 1.04; 95% CI = 1.01-1.09 per 3 parts per million). Exposure to increased levels of ambient PM10 and possibly CO during pregnancy may contribute to the occurrence of preterm births in Southern California.

Epidemiologic studies addressing the relationship between ambient air pollution and fetal development are accumulating worldwide. Studies conducted in China (Wang et al. 1997;Xu et al. 1995), Brazil (Pereira et al. 1998), the Czech Republic (Bobak and Leon 1999;Dejmek et al. 1999;Perera et al. 1999), Mexico (Loomis et al. 1999), Korea (Ha et al. 2001), and the United States (Woodruff et al. 1997) linked ambient air pollution exposure during pregnancy with term low birth weight (LBW), intrauterine growth retardation (IUGR), preterm birth, and perinatal mortality. We recently reported that increases in carbon monoxide, particulate matter < 10 µm in aerodynamic diameter (PM 10 ), and ozone concentrations during vulnerable pregnancy periods increased the risk of term LBW (Ritz and Yu 1999), preterm delivery (Ritz et al. 2000), and certain cardiac malformations, such as ventricular septal defects (Ritz et al. 2002). CO is released directly in motor vehicle exhaust and does not react readily in the atmosphere to form other compounds. Fine (< 2.5 µm) and ultrafine (< 0.1 µm) particles are also released directly in vehicle exhaust but undergo physical and chemical transformations in the atmosphere as they disperse from the roadway (Zhu et al. 2002). The consistently observed associations between ambient CO concentrations and adverse birth outcomes in our previous studies suggest that compounds in motor vehicle exhaust (either CO or associated compounds such as fine and ultrafine particles) may affect fetal development.In our previous studies (Ritz and Yu 1999;Ritz et al. 2000Ritz et al. , 2002, air pollution exposure assessment was based on measurements taken at ambient monitoring stations during specific pregnancy periods. Although such measures may adequately reflect average exposure of pregnant women to background air pollution concentrations in their neighborhood, they may not take into account differential exposure within neighborhoods due to proximity to heavy-traffic roadways and freeways. Women residing closer to these sources may experience greater exposure to potentially toxic compounds released directly in vehicle exhaust or formed in the atmosphere adjacent to roadways. Therefore, we examined whether residential proximity to heavy-traffic roadways, such as freeways and major arterials, during pregnancy was associated with the risk of term LBW and preterm birth in infants born to women living in Los Angeles County, California, between 1994-1996 using a case-control study design. MethodsSubjects. We used birth certificates, provided by the California Department of Health Services (Sacramento, CA), to identify study subjects and to determine their gestational age, birth weight, and values for covariates included in our analyses. We included infants born to women living in the 28 Los Angeles County zip codes evaluated in earlier work (Ritz and Yu 1999;Ritz et al. 2000) and 84 additional zip codes selected to capture areas intersected by freeways and major arterials and collectors (Figure 1). Overall we included...

Context: Epidemiologic studies have reported that cigarette smoking is inversely associated with Parkinson disease (PD). However, questions remain regarding the effect of age at smoking onset, time since quitting, and race/ ethnicity that have not been addressed due to sample size constraints. This comprehensive assessment of the apparent reduced risk of PD associated with smoking may provide important leads for treatment and prevention.Objective: To determine whether race/ethnicity, sex, education, age at diagnosis, and type of tobacco modify the observed effects of smoking on PD. Design, Setting, and Participants: We conducted the first ever pooled analysis of PD combining individuallevel data from 8 US case-control and 3 cohort studies (Nurses' Health Study, Health Professionals Follow-Up Study, and Honolulu-Asia Aging Study) conducted between 1960 and 2004. Case-control studies provided data for 2328 PD cases and 4113 controls matched by age, sex, and ethnicity; cohort studies contributed 488 cases and 4880 controls selected from age-and sex-matched risk sets. Main Outcome Measure: Incident PD.Results: We confirmed inverse associations between PD and smoking and found these to be generally stronger in current compared with former smokers; the associations were stronger in cohort than in case-control studies. We observed inverse trends with pack-years smoked at every age at onset except the very elderly (Ͼ75 years of age), and the reduction of risk lessened with years since quitting smoking. The risk reductions we observed for white and Asian patients were not seen in Hispanic and African American patients. We also found an inverse association both for smoking cigars and/or pipes and for chewing tobacco in male subjects. Conclusions: Our data support a dose-dependent reduction of PD risk associated with cigarette smoking and potentially with other types of tobacco use. Importantly, effects seemed not to be influenced by sex or education. Differences observed by race and age at diagnosis warrant further study.

BackgroundPreeclampsia is a major complication of pregnancy that can lead to substantial maternal and perinatal morbidity, mortality, and preterm birth. Increasing evidence suggests that air pollution adversely affects pregnancy outcomes. Yet few studies have examined how local traffic-generated emissions affect preeclampsia in addition to preterm birth.ObjectivesWe examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD).MethodsWe identified 81,186 singleton birth records from four hospitals (1997–2006) in Los Angeles and Orange Counties, California (USA). We used a line-source dispersion model (CALINE4) to estimate individual exposure to local traffic-generated nitrogen oxides (NOx) and particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) across the entire pregnancy. We used logistic regression to estimate effects of air pollution exposures on preeclampsia, PTD (gestational age < 37 weeks), moderate PTD (MPTD; gestational age < 35 weeks), and very PTD (VPTD; gestational age < 30 weeks).ResultsWe observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NOx and PM2.5. The risk of preeclampsia increased 33% [odds ratio (OR) = 1.33; 95% confidence interval (CI), 1.18–1.49] and 42% (OR = 1.42; 95% CI, 1.26–1.59) for the highest NOx and PM2.5 exposure quartiles, respectively. The risk of VPTD increased 128% (OR = 2.28; 95% CI, 2.15–2.42) and 81% (OR = 1.81; 95% CI, 1.71–1.92) for women in the highest NOx and PM2.5 exposure quartiles, respectively.ConclusionExposure to local traffic-generated air pollution during pregnancy increases the risk of preeclampsia and preterm birth in Southern California women. These results provide further evidence that air pollution is associated with adverse reproductive outcomes.

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Preterm birth may be affected by the interaction of residential air pollution with neighborhood economic hardship. The authors examined variations in traffic-related pollution exposure--measured by distance-weighted traffic density--using a framework reflecting the social and physical environments. An adverse social environment was conceptualized as low socioeconomic status (SES) neighborhoods--census tracts with concentrated poverty, unemployment, and dependence on public assistance. An adverse physical environment was depicted by the winter season, when thermal inversions trap motor vehicle pollutants, thereby increasing traffic-related air pollution. Los Angeles County, California, birth records from 1994 to 1996 were linked to traffic counts, census data, and ambient air pollution measures. The authors fit multivariate logistic models of preterm birth, stratified by neighborhood SES and third pregnancy trimester season. Traffic-related air pollution exposure disproportionately affected low SES neighborhoods in the winter. Further, in these poorer neighborhoods, the winter season evidenced increased susceptibility among women with known risk factors. Health insurance was most beneficial to women residing in neighborhoods exposed to economic hardship and an adverse physical environment. Reducing preterm births warrants a concerted effort of social, economic, and environmental policies, focused on not only individual risk factors but also the reduction of localized air pollution, expansion of health-care coverage, and improvement of neighborhood resources.

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 offspring’s 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.