PubMed Health⌕ Search

Biomedical subjects

Mary H Ward

Publications and source records attributed to Mary H Ward.

At least 19 recordsLinked to original sources

Does the evidence about health risks associated with nitrate ingestion warrant an increase of the nitrate standard for drinking water?

Several authors have suggested that it is safe to raise the health standard for nitrate in drinking water, and save money on measures associated with nitrate pollution of drinking water resources. The major argument has been that the epidemiologic evidence for acute and chronic health effects related to drinking water nitrate at concentrations near the health standard is inconclusive. With respect to the chronic effects, the argument was motivated by the absence of evidence for adverse health effects related to ingestion of nitrate from dietary sources. An interdisciplinary discussion of these arguments led to three important observations. First, there have been only a few well-designed epidemiologic studies that evaluated ingestion of nitrate in drinking water and risk of specific cancers or adverse reproductive outcomes among potentially susceptible subgroups likely to have elevated endogenous nitrosation. Positive associations have been observed for some but not all health outcomes evaluated. Second, the epidemiologic studies of cancer do not support an association between ingestion of dietary nitrate (vegetables) and an increased risk of cancer, because intake of dietary nitrate is associated with intake of antioxidants and other beneficial phytochemicals. Third, 2-3 % of the population in Western Europe and the US could be exposed to nitrate levels in drinking water exceeding the WHO standard of 50 mg/l nitrate, particularly those living in rural areas. The health losses due to this exposure cannot be estimated. Therefore, we conclude that it is not possible to weigh the costs and benefits from changing the nitrate standard for drinking water and groundwater resources by considering the potential consequences for human health and by considering the potential savings due to reduced costs for nitrate removal and prevention of nitrate pollution.

Diet↗

Impaired lung function and lung cancer incidence in a cohort of Swedish construction workers.

BACKGROUND: Although impaired lung function in general has been associated with an increased risk of lung cancer, past studies typically have not attempted to investigate separately the obstructive and restrictive components of respiratory impairment. To deal with this question further, data from a large (n = 176 997) cohort of male Swedish construction workers, for whom spirometry measurements before follow-up were available, were analysed. METHODS: Cancer incidence for 1971-2001 was obtained through linkage with the national cancer registry. Using a modification of the Global Initiative for Chronic Obstructive Lung Disease criteria for chronic obstructive pulmonary disease (COPD), subjects were classified into five categories of lung function: normal, mild COPD, moderate COPD, severe COPD and restrictive lung disease (RLD). Rate ratios (RR) and 95% confidence intervals (CI) for lung cancer across lung function categories were calculated using Poisson regression, adjusted for age and smoking. Other end points (histological types of lung cancer, non-lung tobacco-related cancers, other cancers, total mortality) were also investigated. RESULTS: 834 incident cases of lung cancer were identified. Increased rates of lung cancer were observed for both COPD (mild: RR 1.5, 95% CI 1.2 to 1.9; moderate/severe: RR 2.2, 95% CI 1.8 to 2.7) and RLD (RR 2.0, 95% CI 1.6 to 2.5) relative to normal lung function. These associations did not meaningfully change on applying follow-up lag times of 5, 10 and 15 years after spirometry. When analysed by histological type, associations with both COPD and RLD were stronger for squamous cell carcinoma and small cell carcinoma, and weaker for adenocarcinoma. Both COPD and RLD were associated with increased rates of total mortality. CONCLUSIONS: Obstructive and restrictive impairments in lung function are associated with increased lung cancer risk.

Adult↗

Geographically based investigation of prostate cancer mortality in four U.S. Northern Plain states.

BACKGROUND: Historically, prostate cancer mortality rates have been elevated in the U.S. Northern Plains states. The purpose of this study was to investigate possible contributing factors, especially whether there was any association with crop patterns. METHODS: Prostate cancer mortality rates (1950-2000) in four northern plains states (MN, MT, ND, and SD) were compared to rates for 46 other U.S. states. Within the four states, county rates in urban, less urban, and rural areas also were compared. For additional analysis, urban counties and counties with <10% of county area in crops were excluded. The average percent of county area in total cropland 1930-1950 and 1954-1974 was estimated. Using Poisson regression, we investigated whether the average percentage of county area in total cropland, 1930-1950 and 1954-1974, was associated with prostate cancer mortality rates, 1975-2000, respectively. Poisson regression analyses were also used to evaluate associations between rates and major crops, which included spring and durum wheat, winter wheat, corn, and other crops. Population centroids of the Census 2000 block groups were used to estimate the percentage of males aged 35 and older residing in close proximity to small grains crops. RESULTS: Mortality rates were higher in rural compared to urban counties in 1950-2000 (rate ratio [RR]=1.032; 95% CI=1.001-1.063). Rates in 1950-1974 were significantly associated with production of corn and other crops in 1930-1950 (corn: RR per 10% increase=1.033, 95% CI=1.012-1.054; other crops: RR=1.042, 95% CI=1.021-1.063). Mortality rates in 1975-2000 were significantly associated with spring and durum wheat production in 1954-1974 (RR per 10% increase=1.042, 95% CI=1.017-1.067). Prostate cancer mortality rates increased as the percentage of population living within 500 m of small grains crops increased. CONCLUSIONS: Epidemiologic studies to evaluate agricultural practices are warranted to further evaluate the observed associations.

Adult↗

Vegetables, fruit, and antioxidant-related nutrients and risk of non-Hodgkin lymphoma: a National Cancer Institute-Surveillance, Epidemiology, and End Results population-based case-control study.

BACKGROUND: Factors related to DNA damage and altered immunologic responses, such as reactive oxygen species production, are associated with the risk of non-Hodgkin lymphoma (NHL). OBJECTIVE: The aim was to evaluate NHL risk with intakes of vegetables, fruit, and nutrients involved in antioxidant activities. DESIGN: Incident case subjects aged 20-74 y were identified between 1998 and 2000 from a National Cancer Institute-sponsored study by using four Surveillance, Epidemiology, and End Results registries. Control subjects, who were selected by random dialing (< 65 y) and from Medicare files (> or = 65 y), were matched to cases by age, center, race, and sex. Of 1321 case and 1057 control subjects who enrolled, dietary data were collected on a subset (466 cases and 391 controls). Carotenoid intakes were estimated by using updated values from the US Department of Agriculture nutrient databases. Unconditional logistic regression models were used to estimate odds ratios (ORs) and 95% CIs. RESULTS: NHL risk was inversely associated with higher number of weekly servings of all vegetables (multivariable OR for highest compared with lowest quartile: 0.58; 95% CI: 0.35, 0.95; P for trend = 0.04), green leafy vegetables (OR: 0.59; 95% CI: 0.36, 0.96; P for trend = 0.01), and cruciferous vegetables (OR: 0.62; 95% CI: 0.39, 1.00; P for trend = 0.05) and with higher daily intakes of lutein and zeaxanthin (OR: 0.54; 95% CI: 0.32, 0.91; P for trend = 0.06) and zinc (OR: 0.58; 95% CI: 0.36, 0.91; P for trend = 0.02). An effect modification by exercise and NHL subtype was observed with some food groups and nutrients. CONCLUSION: Higher intakes of vegetables, lutein and zeaxanthin, and zinc are associated with a lower NHL risk.

Adult↗

Risk of non-Hodgkin lymphoma and nitrate and nitrite from drinking water and diet.

INTRODUCTION: Nitrate and nitrite are precursors in the in vivo formation of N-nitroso compounds, potent animal carcinogens. METHODS: We conducted a population-based case-control study of non-Hodgkin lymphoma (NHL) in 1998 to 2000 in Iowa, Detroit, Seattle, and Los Angeles. Because nitrate levels were elevated in many drinking water supplies in Iowa, but not in the other study centers, we evaluated water nitrate levels and risk of NHL in Iowa only. Monitoring data for public supplies were linked to water source histories from 1960 onward. Nitrate was measured at interview homes with private wells. We limited most analyses to those with nitrate estimates for > 70% of their person-years since 1960 (181 cases, 142 controls). For those in the diet arm of the study (458 cases, 383 controls from 4 centers) and for Iowa participants in both the diet and drinking water analyses, we estimated dietary nitrate and nitrite intake using a 117-item food-frequency questionnaire that included foods high in nitrate and nitrite. Odds ratios and 95% confidence intervals were calculated using logistic regression, adjusting for the study matching factors, education, and caloric intake (diet analyses only). RESULTS: We found no overall association with the highest quartile of average drinking water nitrate (> 2.90 mg/L nitrate-N: odds ratios = 1.2; 95% confidence interval = 0.6-2.2) or with years > or = 5 mg/L (10+ years: 1.4; 0.7-2.9). We observed no evidence of an interaction between drinking water nitrate exposure and either vitamin C or red meat intake, an inhibitor and precursor, respectively, of N-nitroso compound formation. Among those in the diet arm, dietary nitrate was inversely associated with risk of NHL (highest quartile: 0.54; 0.34-0.86). Dietary nitrite intake was associated with increasing risk (highest quartile: 3.1; 1.7-5.5) largely due to intakes of bread and cereal sources of nitrite. CONCLUSION: Average drinking water nitrate levels below 3 mg/L were not associated with NHL risk. Our study had limited power to evaluate higher levels that deserve further study.

Aged↗

Proximity to crops and residential exposure to agricultural herbicides in iowa.

Rural residents can be exposed to agricultural pesticides through the proximity of their homes to crop fields. Previously, we developed a method to create historical crop maps using a geographic information system. The aim of the present study was to determine whether crop maps are useful for predicting levels of crop herbicides in carpet dust samples from residences. From homes of participants in a case-control study of non-Hodgkin lymphoma in Iowa (1998-2000), we collected vacuum cleaner dust and measured 14 herbicides with high use on corn and soybeans in Iowa. Of 112 homes, 58% of residences had crops within 500 m of their home, an intermediate distance for primary drift from aerial and ground applications. Detection rates for herbicides ranged from 0% for metribuzin and cyanazine to 95% for 2,4-dichlorophenoxyacetic acid. Six herbicides used almost exclusively in agriculture were detected in 28% of homes. Detections and concentrations were highest in homes with an active farmer. Increasing acreage of corn and soybean fields within 750 m of homes was associated with significantly elevated odds of detecting agricultural herbicides compared with homes with no crops within 750 m (adjusted odds ratio per 10 acres = 1.06; 95% confidence interval, 1.02-1.11). Herbicide concentrations also increased significantly with increasing acreage within 750 m. We evaluated the distance of crop fields from the home at < 100, 101-250, 251-500, and 501-750 m. Including the crop buffer distance parameters in the model did not significantly improve the fit compared with a model with total acres within 750 m. Our results indicate that crop maps may be a useful method for estimating levels of herbicides in homes from nearby crop fields.

Case-Control Studies↗

Meat and meat-mutagen intake and risk of non-Hodgkin lymphoma: results from a NCI-SEER case-control study.

Non-Hodgkin Lymphoma (NHL) incidence has risen dramatically over past decades, but the reasons for most of this increase are not known. Meat cooked well-done using high-temperature cooking techniques produces heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (B[a]P). This study was conducted as a population-based case-control study in Iowa, Detroit, Seattle and Los Angeles and was designed to determine whether meat, meat-cooking methods, HCAs or PAHs from meat were associated with NHL risk. This study consisted of 458 NHL cases, diagnosed between 1998 and 2000, and 383 controls. Participants completed a 117-item food frequency questionnaire (FFQ), with graphical aids to assess the meat-cooking method and doneness level, which was linked to a HCA and B[a]P database. Logistic regression, comparing the fourth to the first quartile, found no association between red meat or processed meat intake and risk for NHL [odds ratio (OR) and 95% confidence interval (CI): 1.10 (0.67-1.81) and 1.18 (0.74-1.89), respectively]. A marginally significant elevated risk for NHL was associated with broiled meat [OR and 95% CI: 1.32 (0.99-1.77); P trend = 0.09], comparing those who consumed broiled meat with those who did not. The degree to which meat was cooked was not associated with the risk for NHL, although one of the HCAs, DiMeIQx (2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline), was associated with an inverse risk. Fat intake was associated with a significantly elevated risk for NHL [OR and 95% CI: 1.60 (1.05-2.45); P trend = 0.12]; in contrast, animal protein was inversely associated with risk for NHL [OR and 95% CI: 0.39 (0.22-0.70); P trend = 0.004]. Overall, our study suggests that consumption of meat, whether or not it is well-done, does not increase the risk of NHL. Furthermore, neither HCAs nor B[a]P from meat increase the risk of NHL.

Adult↗

Hair dyes and risk of glioma among Nebraska women.

The etiology of brain cancer is not well understood. We conducted a population-based case-control study among 112 white women in Nebraska who were newly diagnosed with glioma between July 1988 and June 1993, and 215 controls, to identify risk factors for this disease. A 1.7-fold increased risk of glioma was observed for women who ever used hair coloring products (95% confidence interval (CI) = 1.0-2.9, 62 cases), and a 2.4-fold risk for those who used permanent hair coloring products (odds ratio (OR) = 2.4, 95% CI = 1.3-4.5, 39 cases). For women with the most aggressive form of glioma, glioblastoma multiforme, risk increased with duration of exposure to 4.9 (95% CI = 1.6-15.7, 10 cases) after 21 or more years of permanent hair coloring use. Higher risks were observed with earlier age at first use, but we did not see an exposure-response pattern with frequency of use of permanent dyes. No association was observed with use of non-permanent (sometimes called temporary or semi-permanent) hair coloring products. These suggestive findings need confirmation in future studies with larger sample sizes, fewer proxy respondents, and the ability to evaluate the effect of changes in formulations over time.

Adult↗

Positional accuracy of two methods of geocoding.

BACKGROUND: Geocoding is often used in epidemiologic studies to map residences with geographic information systems (GIS). The accuracy of the method is usually not determined. METHODS: We collected global positioning system (GPS) measurements at homes in a case-control study of non-Hodgkin lymphoma in Iowa. We geocoded the addresses by 2 methods: (1) in-house, using ArcView 3.2 software and the U.S. Census Bureau TIGER 2000 street database; and (2) automated geocoding by a commercial firm. We calculated the distance between the geocoded and GPS location (positional error) overall and separately for homes within towns and outside (rural). We evaluated the error in classifying homes with respect to their proximity to crop fields. RESULTS: Overall, the majority of homes were geocoded with positional errors of less than 100 m by both methods (ArcView/TIGER 2000, median = 62 m [interquartile range = 39-103]; commercial firm, median = 61 m [interquartile range = 35-137]). For town residences, the percent geocoded with errors of </=100 m was 81% for ArcView/TIGER 2000 and 84% for the commercial firm. For rural residences, a smaller percent of addresses were geocoded with this level of accuracy, especially by the commercial firm (ArcView/TIGER 2000, 56%; commercial firm, 28%). Geocoding errors affected our classification of homes according to their proximity to agricultural fields at 100 m, but not at greater distances (250-500 m). CONCLUSIONS: Our results indicate greater positional errors for rural addresses compared with town addresses. Using a commercial firm did not improve accuracy compared with our in-house method. The effect of geocoding errors on exposure classification will depend on the spatial variation of the exposure being studied.

Adult↗

Drinking water and dietary sources of nitrate and nitrite and risk of glioma.

OBJECTIVE: Dietary nitrite has been associated with increased glioma risk; however, drinking water nitrate has not been extensively evaluated. METHODS: We conducted a population-based case-control study of adult glioma in Nebraska. Water utility nitrate measurements were linked to residential water source histories. We computed average nitrate exposure over a 20-year period. A food frequency questionnaire was used to assess dietary nitrate and nitrite. RESULTS: Increasing quartiles of the average nitrate level in drinking water were not significantly associated with risk (adjusted odd ratios: 1.4, 1.2, 1.3). Risk was similar among those with both higher and lower intakes of vitamin C, an inhibitor of N-nitroso compound formation. Dietary nitrite intake was not associated with risk. CONCLUSIONS: Our study does not support a role for drinking water and dietary sources of nitrate and nitrite in risk of adult glioma.

Aged↗

Workgroup report: Drinking-water nitrate and health--recent findings and research needs.

Human alteration of the nitrogen cycle has resulted in steadily accumulating nitrate in our water resources. The U.S. maximum contaminant level and World Health Organization guidelines for nitrate in drinking water were promulgated to protect infants from developing methemoglobinemia, an acute condition. Some scientists have recently suggested that the regulatory limit for nitrate is overly conservative; however, they have not thoroughly considered chronic health outcomes. In August 2004, a symposium on drinking-water nitrate and health was held at the International Society for Environmental Epidemiology meeting to evaluate nitrate exposures and associated health effects in relation to the current regulatory limit. The contribution of drinking-water nitrate toward endogenous formation of N-nitroso compounds was evaluated with a focus toward identifying subpopulations with increased rates of nitrosation. Adverse health effects may be the result of a complex interaction of the amount of nitrate ingested, the concomitant ingestion of nitrosation cofactors and precursors, and specific medical conditions that increase nitrosation. Workshop participants concluded that more experimental studies are needed and that a particularly fruitful approach may be to conduct epidemiologic studies among susceptible subgroups with increased endogenous nitrosation. The few epidemiologic studies that have evaluated intake of nitrosation precursors and/or nitrosation inhibitors have observed elevated risks for colon cancer and neural tube defects associated with drinking-water nitrate concentrations below the regulatory limit. The role of drinking-water nitrate exposure as a risk factor for specific cancers, reproductive outcomes, and other chronic health effects must be studied more thoroughly before changes to the regulatory level for nitrate in drinking water can be considered.

Drinking↗

Current practices in spatial analysis of cancer data: data characteristics and data sources for geographic studies of cancer.

The use of spatially referenced data in cancer studies is gaining in prominence, fueled by the development and availability of spatial analytic tools and the broadening recognition of the linkages between geography and health. We provide an overview of some of the unique characteristics of spatial data, followed by an account of the major types and sources of data used in the spatial analysis of cancer, including data from cancer registries, population data, health surveys, environmental data, and remote sensing data. We cite numerous examples of recent studies that have used these data, with a focus on etiological research.

Journal Article↗

Pancreatic cancer and drinking water and dietary sources of nitrate and nitrite.

N-Nitroso compounds, known animal carcinogens, are formed endogenously from drinking water and dietary sources of nitrate and nitrite. The authors conducted a population-based case-control study of pancreatic cancer in Iowa to determine whether increased consumption of nitrate and nitrite from drinking water and dietary sources was associated with risk. They linked detailed water source histories to nitrate measurements for Iowa community water supplies. After exclusions for insufficient data, 1,244 controls and 189 pancreatic cancer cases were available for analysis. Among controls, the median average nitrate level (1960-1987) was 1.27 (interquartile range, 0.6-2.8) mg of nitrate nitrogen per liter of water. No association was observed between pancreatic cancer risk and increasing quartiles of the community water supplies' nitrate level. Increasing intake of dietary nitrite from animal sources was associated with an elevated risk of pancreatic cancer among men and women (highest quartile odds ratios = 2.3, 95% confidence interval: 1.1, 5.1, for men and 3.2, 95% confidence interval: 1.6, 6.4, for women). In contrast, dietary nitrate intake showed an inverse association with risk among women and no association among men. This study suggests that long-term exposure to drinking water nitrate at levels below the maximum contaminant level of nitrate nitrogen (10 mg/liter) is not associated with pancreatic cancer; however, the consumption of dietary nitrite from animal products may increase risk.

Adult↗

Using geographic information systems for exposure assessment in environmental epidemiology studies.

Geographic information systems (GIS) are being used with increasing frequency in environmental epidemiology studies. Reported applications include locating the study population by geocoding addresses (assigning mapping coordinates), using proximity analysis of contaminant source as a surrogate for exposure, and integrating environmental monitoring data into the analysis of the health outcomes. Although most of these studies have been ecologic in design, some have used GIS in estimating environmental levels of a contaminant at the individual level and to design exposure metrics for use in epidemiologic studies. In this article we discuss fundamentals of three scientific disciplines instrumental to using GIS in exposure assessment for epidemiologic studies: geospatial science, environmental science, and epidemiology. We also explore how a GIS can be used to accomplish several steps in the exposure assessment process. These steps include defining the study population, identifying source and potential routes of exposure, estimating environmental levels of target contaminants, and estimating personal exposures. We present and discuss examples for the first three steps. We discuss potential use of GIS and global positioning systems (GPS) in the last step. On the basis of our findings, we conclude that the use of GIS in exposure assessment for environmental epidemiology studies is not only feasible but can enhance the understanding of the association between contaminants in our environment and disease.

Cluster Analysis↗

Nitrate in public water supplies and risk of bladder cancer.

BACKGROUND: Nitrate is a precursor compound in the formation of N-nitroso compounds, most of which are potent animal carcinogens. N-nitroso compounds and their precursors have not been extensively evaluated as bladder cancer risk factors. METHODS: We conducted a population-based case-control study of bladder cancer in Iowa. Cases were men and women newly diagnosed with bladder cancer in 1986-1989. Nitrate data for Iowa public water supplies were sparse before the 1960s. To reduce misclassification by unknown nitrate levels, we included only those who used public supplies with nitrate data for 70% or more of their person-years since 1960 (808 cases, 1259 controls). RESULTS: Among controls, the median average nitrate level for their Iowa residences with public water supplies was 1.3 mg/liter nitrate-nitrogen (interquartile range = 0.6-3.0). After adjustment for confounders, we found no increased risk of bladder cancer with increasing average nitrate levels in drinking water; the highest quartile odds ratio for women was 0.8 (95% confidence interval = 0.4-0.8), and for men 0.5 (0.4-0.8). We observed no association among those with high water nitrate exposure (>median) and low (<median) vitamin C intake compared with those who had low water nitrate and high vitamin C intake. CONCLUSIONS: Our data suggest that long-term exposure to nitrate in drinking water at levels in this study (90th percentile 5.5 mg/liter nitrate-nitrogen) is not associated with risk of bladder cancer.

Adult↗

Nitrate in public water supplies and the risk of colon and rectum cancers.

BACKGROUND: Nitrate is a widespread contaminant of drinking water, but its potential health effects are unclear. In the body, nitrate is reduced to nitrite, which can react with amines and amides by nitrosation to form N-nitroso compounds, known animal carcinogens. N-nitroso compound formation is inhibited by certain nutrients, such as vitamin C, and increased by meat intake. METHODS: We investigated the association of nitrate in public water supplies with incident colon and rectum cancers in a case-control study conducted in Iowa from 1986 to 1989. Nitrate levels in Iowa towns were linked to the participants' water source histories. We focused our analyses on the period from 1960 onward, during which nitrate measurements were more frequent, and we restricted analyses to those persons with public water supplies that had nitrate data (actual or imputed) for greater than 70% of this time period (376 colon cancer cases, 338 rectum cancer cases, and 1244 controls). RESULTS: There were negligible overall associations of colon or rectum cancers with measures of nitrate in public water supplies, including average nitrate and the number of years with elevated average nitrate levels. For more than 10 years with average nitrate greater than 5 mg/L, the odds ratio (OR) for colon cancer was 1.2 (95% confidence interval [CI] = 0.9-1.6) and for rectum the OR was 1.1 (CI = 0.7-1.5). However, nitrate exposure (>10 years with average nitrate >5 mg/L) was associated with increased colon cancer risk among subgroups with low vitamin C intake (OR = 2.0; CI = 1.2-3.3) and high meat intake (OR = 2.2; CI = 1.4-3.6). These patterns were not observed for rectum cancer. CONCLUSIONS: Our analyses suggest that any increased risk of colon cancer associated with nitrate in public water supplies might occur only among susceptible subpopulations.

Adult↗