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Beate Ritz

Publications and source records attributed to Beate Ritz.

25 records · Page 2Linked to original sources

Can lessons from public health disease surveillance be applied to environmental public health tracking?

Disease surveillance has a century-long tradition in public health, and environmental data have been collected at a national level by the U.S. Environmental Protection Agency for several decades. Recently, the Centers for Disease Control and Prevention announced an initiative to develop a national environmental public health tracking (EPHT) network with "linkage" of existing environmental and chronic disease data as a central goal. On the basis of experience with long-established disease surveillance systems, in this article we suggest how a system capable of linking routinely collected disease and exposure data should be developed, but caution that formal linkage of data is not the only approach required for an effective EPHT program. The primary operational goal of EPHT has to be the "treatment" of the environment to prevent and/or reduce exposures and minimize population risk for developing chronic diseases. Chronic, multifactorial diseases do not lend themselves to data-driven evaluations of intervention strategies, time trends, exposure patterns, or identification of at-risk populations based only on routinely collected surveillance data. Thus, EPHT should be synonymous with a dynamic process requiring regular system updates to a) incorporate new technologies to improve population-level exposure and disease assessment, b) allow public dissemination of new data that become available, c) allow the policy community to address new and emerging exposures and disease "threads," and d) evaluate the effectiveness of EPHT over some appropriate time interval. It will be necessary to weigh the benefits of surveillance against its costs, but the major challenge will be to maintain support for this important new system. Key words: environmental health, evaluation, intervention, registries, surveillance.

Chronic Disease↗

Local variations in CO and particulate air pollution and adverse birth outcomes in Los Angeles County, California, USA.

We extended our previous analyses of term low birth weight (LBW) and preterm birth to 1994-2000, a period of declining air pollution levels in the South Coast Air Basin. We speculated that the effects we observed previously for carbon monoxide, particulate matter < 10 microm in aerodynamic diameter (PM10), and traffic density were attributable to toxins sorbed to primary exhaust particles. Focusing on CO, PM10, and particulate matter < 2.5 microm in aerodynamic diameter (PM2.5), we examined whether varying residential distances from monitoring stations affected risk estimates, because effect attenuation may result from local pollutant heterogeneity inadequately captured by ambient stations. We geocoded home locations, calculated the distance to the nearest air monitors, estimated exposure levels by pregnancy period, and performed logistic regression analyses for subjects living within 1-4 mi of a station. For women residing within a 1-mi distance, we observed a 27% increase in risk for high (> or = 75th percentile) first-trimester CO exposures and preterm birth and a 36% increase for high third-trimester pregnancy CO exposures and term LBW. For particles, we observed similar size effects during early and late pregnancy for both term LBW and preterm birth. In contrast, smaller or no effects were observed beyond a 1-mi distance of a residence from a station. Associations between CO and PM10 averaged over the whole pregnancy and term LBW were generally smaller than effects for early and late pregnancy. These new results for 1994-2000 generally confirm our previous observations for the period 1989-1993, again linking CO and particle exposures to term LBW and preterm birth. In addition, they confirm our suspicions about having to address local heterogeneity for these pollutants in Los Angeles.

Adult↗

Pancreatic cancer mortality and organochlorine pesticide exposure in California, 1989-1996.

BACKGROUND: Occupational studies have suggested a possible link between organochlorine pesticides and the occurrence of pancreatic cancers. California maintains a death file and a pesticide reporting system that allows examination of this relationship for residents of high use areas. METHODS: We employed a mortality odds ratio design to compare deaths from pancreatic cancer (1989-1996) with a random sample of non-cancer deaths. Using pesticide data for three agricultural counties, we classified 102 ZIP codes in quartiles of pesticide usage for 1972-1989. Using logistic regression we estimated the effect of pesticide applications by ZIP code controlling for possible confounders. RESULTS: Among long-term residents, pancreatic cancer mortality was elevated for those living in ZIP codes with the highest use of four pesticides: 1,3-dichloropropene (1,3-d), captafol, pentachloronitrobenzene (PCNB), and dieldrin. No dose-response relationship was observed. CONCLUSIONS: Our study suggests increased pancreatic cancer mortality among long-term residents in areas of high application rates of 1,3-d (an EPA-classified probable human carcinogen), captafol, pentacholoronitrobenzene (PCNB), and dieldrin.

Age Factors↗

Residential proximity to traffic and adverse birth outcomes in Los Angeles county, California, 1994-1996.

We reported previously that increases in ambient air pollution in the Los Angeles basin increased the risk of low weight and premature birth. However, ambient concentrations measured at monitoring stations may not take into account differential exposure to pollutants found in elevated concentrations near heavy-traffic roadways. Therefore, we used an epidemiologic case-control study design to examine whether residential proximity to heavy-traffic roadways influenced the occurrence of low birth weight (LBW) and/or preterm birth in Los Angeles County between 1994 and 1996. We mapped subject home locations at birth and estimated exposure to traffic-related air pollution using a distance-weighted traffic density (DWTD) measure. This measure takes into account residential proximity to and level of traffic on roadways surrounding homes. We calculated odds ratios (ORs) and risk ratios (RRs) for being LBW and/or preterm per quintile of DWTD. The clearest exposure-response pattern was observed for preterm birth, with an RR of 1.08 [95% confidence interval (CI), 1.01-1.15] for infants in the highest DWTD quintile. Although higher risks were observed for LBW infants, exposure-response relations were less consistent. Examining the influence of season, we found elevated risks primarily for women whose third trimester fell during fall/winter months (OR(term LBW) = 1.39; 95% CI, 1.16-1.67; OR(preterm and LBW) = 1.24; 95% CI = 1.03-1.48; RR(all preterm) = 1.15; 95% CI, 1.05-1.26), and exposure-response relations were stronger for all outcomes. This result is consistent with elevated pollution in proximity to sources during more stagnant air conditions present in winter months. Our previous research and these latest results suggest exposure to traffic-related pollutants may be important.

Adult↗

Historical pesticide exposure in California using pesticide use reports and land-use surveys: an assessment of misclassification error and bias.

We used California's Pesticide Use Report (PUR) and land-use survey data to conduct a simulation study evaluating the potential consequences of misclassifying residential exposure from proximity to agricultural pesticide application in health effect studies. We developed a geographic model linking the PUR with crop location data from land-use surveys to assess the impact of exposure misclassification from simpler exposure models based solely on PUR or land-use data. We simulated the random selection of population controls recruited into a hypothetical case-control study within an agricultural region. Using residential parcel data, we derived annual exposure prevalences, sensitivity, and specificity for five pesticides and relied on the PUR plus land-use model as the "gold standard." Based on these estimates, we calculated the attenuation of prespecified true odds ratios (ORs), assuming nondifferential exposure misclassification. True ORs were severely attenuated a) when residential exposure status was based on a larger geographic area yielding higher sensitivity but low specificity for exposure, in contrast to relying on a smaller area and increasing specificity; b) for less frequently applied pesticides; and c) with increasing mobility of residents among the study population. Considerable effect estimate attenuation also occurred when we used residential distance to crops as a proxy for pesticide exposure. Finally, exposure classifications based on annual instead of seasonal summaries of PUR resulted in highly attenuated ORs, especially during seasons when applications of specific pesticides were unlikely to occur. These results underscore the importance of increasing the spatiotemporal resolution of pesticide exposure models to minimize misclassification.

Agriculture↗

Ambient air pollution and risk of birth defects in Southern California.

The authors evaluated the effect of air pollution on the occurrence of birth defects ascertained by the California Birth Defects Monitoring Program in neonates and fetuses delivered in southern California in 1987-1993. By using measurements from ambient monitoring stations of carbon monoxide (CO), nitrogen dioxide, ozone, and particulate matter <10 microm in aerodynamic diameter, they calculated average monthly exposure estimates for each pregnancy. Conventional, polytomous, and hierarchical logistic regression was used to estimate odds ratios for subgroups of cardiac and orofacial defects. Odds ratios for cardiac ventricular septal defects increased in a dose-response fashion with increasing second-month CO exposure (odds ratio (OR)(2nd quartile) CO = 1.62, 95% confidence interval (CI): 1.05, 2.48; OR(3rd quartile) CO = 2.09, 95% CI: 1.19, 3.67; OR(4th quartile) CO = 2.95, 95% CI: 1.44, 6.05). Similarly, risks for aortic artery and valve defects, pulmonary artery and valve anomalies, and conotruncal defects increased with second-month ozone exposure. The study was inconclusive for other air pollutants. The authors' results are supported by the specificity of the timing of the effect and some evidence from animal data; however, this is the first known study to link ambient air pollution during a vulnerable window of development to human malformations. Confirmation by further studies is needed.

Air Pollutants↗

Indoor exposure to molds and allergic sensitization.

Evidence that indoor dampness and mold growth are associated with respiratory health has been accumulating, but few studies have been able to examine health risks in relation to measured levels of indoor mold exposure. In particular, little is known about the contribution of indoor molds to the development of allergic sensitization. As a part of an ongoing study examining the effects of ambient air pollutants on respiratory health and atopic diseases in German school children, we examined the relation between viable mold levels indoors and allergic sensitization in 272 children. We examined whether allergic sensitization in children is associated with higher fungal spore count in settled house dust sampled from living room floors. Adjusting for age, sex, parental education, region of residency, and parental history of atopy, we found that mold spore counts for Cladosporium and Aspergillus were associated with an increased risk of allergic sensitization. Sensitized children exposed to high levels of mold spores (> 90th percentile) were more likely to suffer from symptoms of rhinoconjunctivitis. We conclude that elevated indoor concentrations of molds in wintertime might play a role in increasing the risk of developing atopic symptoms and allergic sensitization not only to molds but also to other common, inhaled allergens. These effects were strongest in the group of children who had lived in the same home since birth.

Adolescent↗