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Two U.S. studies found inverse associations between measured exposure to certain pesticides and blood vitamin D levels. They do not show that pesticides cause vitamin D deficiency. Both were cross-sectional analyses, which capture exposure and vitamin D status at a point in time and cannot establish which came first.
What the studies found
The evidence concerns two distinct exposures, not pesticides as a single category: selected organochlorines measured in blood in one study, and glyphosate measured in urine in another.
| Study | Exposure and measure | Participants and data period | Finding |
|---|---|---|---|
| Yang et al., 2012 | Seven organochlorine pesticides measured in serum | 1,275 U.S. adults aged 20 or older; NHANES 2003–2004 | Of the seven pesticides detectable in at least 80% of participants, serum p,p′-DDT, p,p′-DDE, and β-hexachlorocyclohexane had statistically significant inverse associations with serum 25-hydroxyvitamin D (25(OH)D). Read the study. |
| Glyphosate analysis, 2026 | Glyphosate measured in urine | 4,284 participants; NHANES 2013–2018 | The authors reported an inverse association between urinary glyphosate and serum 25(OH)D in adjusted models (β = −4.208, P = 0.009). The coefficient’s clinical meaning depends on the paper’s model and measurement scale; it should not be read as a direct change in an individual’s vitamin D level. Read the study. |
The studies differ in pesticide, biomarker, data period, and sample size. Their results are not directly comparable, and together they do not establish a shared biological mechanism.
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Both studies analyzed existing NHANES data at a single point in time. They show that certain pesticide biomarkers and serum 25(OH)D were associated in those datasets; they did not test whether pesticide exposure caused a person’s vitamin D level to fall. A cross-sectional study cannot establish whether exposure came before the measured vitamin D status, and it cannot rule out residual confounding.
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The 2012 authors described their findings as suggestive and called for prospective and experimental work. The 2026 paper likewise says its analysis cannot establish causality and concludes: “Longitudinal and experimental studies are needed to clarify causality, the underlying mechanisms, and public health implications.”
What counts as vitamin D deficiency?
The NIH Office of Dietary Supplements summarizes the National Academies’ threshold: a serum 25(OH)D concentration below 30 nmol/L (12 ng/mL) indicates risk of deficiency. That threshold describes vitamin D status; it does not identify the reason for a low result or attribute it to pesticide exposure. See the NIH fact sheet.
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What readers can reasonably conclude
- Human data have reported inverse associations for three selected organochlorines and for urinary glyphosate.
- The findings apply to those specific chemicals and measurements, not to every pesticide.
- The available studies do not establish that pesticide exposure causes vitamin D deficiency or explain an individual’s low vitamin D result.
- The glyphosate paper calls for longitudinal studies with repeated measurements and experimental research; the causal question remains unresolved.
These findings alone are not a basis for stopping a food, taking a supplement, buying a home test, or attributing an individual deficiency to pesticides. A vitamin D result cannot by itself identify its cause.
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