Nitrates are a major contaminant of drinking water in agricultural regions and are present in large amounts in some vegetables. Nitrates compete with thyroid uptake of iodide, thus adversely affecting thyroid function.
We examined the association between thyroid cancer, hypothyroidism, and hyperthyroidism in a cohort of 21,977 elderly women enrolled in 1986 in Iowa. 10 years. We used a public database of nitrate measurements (1955–1988) to estimate nitrate ingestion from drinking water. Dietary nitrate intake was estimated using food frequency questionnaires and levels from published literature. Cancer incidence was determined until 2004.
We found an increased risk of thyroid cancer with high mean nitrate levels in public water supplies and water consumption greater than 5 mg/L nitrate-N (>5 mg/L for ≤5 years, relative risk [RR] = 2.6 ). [95% confidence interval (CI) = 1.1-6.2]). We did not observe any association with the prevalence of hypothyroidism or hyperthyroidism. High dietary nitrate intake was associated with an increased risk of thyroid cancer (highest vs. least square, RR = 2.9 [1.0–8.1]; P = 0.046 for trend) and prevalence of hypothyroidism (ratio = 1.2 [95%]). CI = 1.1-1.4]), but not hyperthyroidism.
Nitrates play a role in thyroid cancer and warrants further investigation.
Thyroid cancer is the most common malignancy of the endocrine system and the eighth most common malignancy among women.1 The incidence of thyroid cancer in the United States has increased significantly since 1980, increasing by 6% annually between 1997 and 1997. . 2003.2 This increase may reflect better detection, but recent analyzes of US incidence indicate at least some increase in major cancers and among men and women of all races and ethnicities.4,5 This In addition to detection, other factors are shown.
Papillary thyroid cancer accounts for more than 70% of thyroid tumors in the United States. The only known risk factor is exposure to ionizing radiation, especially in young children.1 Some epidemiological studies have shown an increased risk of goitre, number of pregnancies7, and a lower risk of eating fish and cruciferous vegetables.1,6
Ingested nitrate inhibits thyroid iodide uptake by binding to the sodium-iodide symporter on the surface of thyroid follicles. It decreases levels of the thyroid hormones triiodothyronine (T3) and thyroxine (T4) and increases thyroid-stimulating hormone (TSH). TSH controls thyroid hormone production through a negative feedback loop.8-11 Chronic stimulation of the thyroid gland by TSH leads to proliferative changes in follicular cells, including hypertrophy, hyperplasia, as well as neoplasia.12,13 There is some evidence from human studies. Elevated levels of nitrate in drinking water are associated with increased thyroid size and frequency of thyroid disorders. 14,15 Nitrate and nitrite are also precursors for the endogenous formation of N-nitroso compounds, which are carcinogenic in thyroid-forming animals. and many other cancers in animal models.16 Ingestion of nitrates and nitrites has been associated with an increased risk of gastric, esophageal, and other cancers in some epidemiological studies.17
Nitrate is a common contaminant in drinking water, particularly in agricultural areas where nitrate concentrations in drinking water supplies have increased since the 1950s due to the use of nitrogen fertilizers.18–20 Nitrate is a natural component of the diet and is present at high levels. green leafy vegetables and some root vegetables. There is some evidence that high fertilizer use increases nitrate levels in vegetables.21 For example, organically grown lettuce that does not receive inorganic nitrogen fertilizers has lower nitrate levels than conventionally grown lettuce.22 Therefore, intensive farming practices may have increased. is. exposure to nitrates from food and drinking water sources.
High levels of nitrate poisoning can cause methemoglobinemia in infants. For this reason, nitrate in public water supplies is regulated at a maximum contaminant level (MCL) of 10 mg/L (approximately 45 mg/L as nitrate) as nitrate-nitrogen (N). Special attention was paid to the food level of children, and the permissible daily amount was established for the diet. However, regulatory limits for nitrate in food and water have not been studied in detail in relation to other health outcomes.23 To date, epidemiological studies of thyroid cancer risk have not evaluated nitrate intake in relation to thyroid cancer, and the relationship between
idism in relation to nitrate intake from drinking water and dietary sources in a prospective cohort of older women in Iowa.
Details of the study population have been described previously.24,25 Briefly, a questionnaire was mailed in 1986 to 98,030 women aged between 55 and 69 years who were randomly selected from Iowa driver’s license files. A total of 41,836 women participated in the initial survey, and constituted the study cohort. There were slight demographic differences between respondents and nonrespondents,25 with nonrespondents having slightly higher mortality from smoking-related cancers.25,26
The initial interview contained questions about demographics, anthropometry, reproductive history, hormone use, family history of cancer, residence location, physical activity, smoking, alcohol consumption, and medical conditions. This included questions on whether the respondent had ever taken medication for hypothyroidism and hyperthyroidism, and whether they were currently taking medication for these conditions. The questionnaire also included a 126-item semi-quantitative food frequency questionnaire adapted from the 1984 Nurses Health Study.25,27 Nitrate intake from foods was calculated using the Harvard Nutrient Database updated in 2008 for specific foods. Nitrate levels were assigned by computing means of published values weighted by consumption frequencies for the US population.
Information about the participants’ usual source of drinking water was collected in the second follow-up questionnaire in 1989; a total of 36,127 women (89%) responded. Participants were asked the primary source of their drinking water at their current residence (municipal [public] water supply, private well, bottled water, or other) and how long they drank that type of water (<1 year, 1–5 years, 6–10 years, 11–20 years, >20 years, or unknown). Public supplies were the primary drinking water source (76% of women) followed by private wells (18%) and bottled water or another source (6%). Of women using the public supplies, 82% used the supply for >10 years and 70% used the supply for >20 years.