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Cited by 202Vitamin D Research StudiesEffects and risks of endocrine disrupting chemicalsAntioxidant Activity and Oxidative Stress

Air pollution, environmental chemicals, and smoking may trigger vitamin D deficiency: Evidence and potential mechanisms

Open access
Mousavi, Sayed Esmaeil, Amini, Heresh, Heydarpour, Pouria, Amini Chermahini, Fatemeh, Godderis, Lode·2019·Environment International
DOI 10.1016/j.envint.2018.11.052
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Abstract

Beyond vitamin D (VD) effect on bone homeostasis, numerous physiological functions in human health have been described for this versatile prohormone. In 2016, 95% of the world's population lived in areas where annual mean ambient particulate matter (<2.5 μm) levels exceeded the World Health Organization guideline value (Shaddick et al., 2018). On the other hand, industries disperse thousands of chemicals continually into the environment. Further, considerable fraction of populations are exposed to tobacco smoke. All of these may disrupt biochemical pathways and cause detrimental consequences, such as VD deficiency (VDD). In spite of the remarkable number of studies conducted on the role of some of the above mentioned exposures on VDD, the literature suffers from two main shortcomings: (1) an overview of the impacts of environmental exposures on the levels of main VD metabolites, and (2) credible engaged mechanisms in VDD because of those exposures. To summarize explanations for these unclear topics, we conducted the present review, using relevant keywords in the PubMed database, to investigate the adverse effects of exposure to air pollution, some environmental chemicals, and smoking on the VD metabolism, and incorporate relevant potential pathways disrupting VD endocrine system (VDES) leading to VDD. Air pollution may lead to the reduction of VD cutaneous production either directly by blocking ultraviolet B photons or indirectly by decreasing outdoor activity. Heavy metals may reduce VD serum levels by increasing renal tubular dysfunction, as well as downregulating the transcription of cytochrome P450 mixed-function oxidases (CYPs). Endocrine-disrupting chemicals (EDCs) may inhibit the activity and expression of CYPs, and indirectly cause VDD through weight gain and dysregulation of thyroid hormone, parathyroid hormone, and calcium homeostasis. Smoking through several pathways decreases serum 25(OH)D and 1,25(OH)2D levels, VD intake from diet, and the cutaneous production of VD through skin aging. In summary, disturbance in the cutaneous production of cholecalciferol, decreased intestinal intake of VD, the modulation of genes involved in VD homeostasis, and decreased local production of calcitriol in target tissues are the most likely mechanisms that involve in decreasing the serum VD levels.

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  • Smokers compared with non-smokers show low vitamin D and parathyroid hormone serum levels, exhibiting a suppressive effect of tobacco on production of parathyroid hormone, cholecalciferol, and calcitriol.

    “Epidemiological, in vitro, and in vivo studies have shown that smokers compared to non-smokers, show low vitamin D and PTH serum levels, exhibiting a suppressive effect of tobacco on the production of PTH, cholecalciferol, and calcitriol [32].”

    From Skeletal System Biology and Smoke Damage: From Basic Science to Medical Clinic (2021) · cites this paper as [32]

  • Skin aging is among the mechanisms that could determine the observed decrease in vitamin D levels, as smoking plays a predominant role in the skin aging process.

    “Among the mechanisms that could determine the observed decrease in vitamin D levels, skin aging can be considered, as smoking plays a predominant role in the skin aging process [32].”

    From Skeletal System Biology and Smoke Damage: From Basic Science to Medical Clinic (2021) · cites this paper as [32]

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Research works printed but not linked: 2

  1. Lips, P., van Schoor, N., 2011. Worldwide Vitamin D Status. Vitamin D, Third edition. Elsevier.
  2. Roe, F.J.C., 1993. BOOK REVIEWS. The Annals of Occupational Hygiene. 37. pp. 341.

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Authors
Mousavi, S. E., Amini, H., Heydarpour, P., Amini Chermahini, F., & Godderis, L.
Affiliations
  • Shahrekord University of Medical Sciences (IR)
  • Harvard University (US)
  • Tehran University of Medical Sciences (IR)
  • KU Leuven (BE)
Corresponding author
Mousavi, Sayed Esmaeil
ORCID
Venue
Environment International
Publisher
Elsevier BV
Published
2019-01
Volume
122
Pages
67-90
ISSN
0160-4120 (ISSN-L)
DOI
10.1016/j.envint.2018.11.052
OpenAlex
W2903481631
Cited by
202
References
173
Citations by year
2026: 13 · 2025: 33 · 2024: 32 · 2023: 28 · 2022: 27 · 2021: 34 · 2020: 20 · 2019: 15
FWCI
2.55
Type
journal article
Language
en
Open access
Licence
Locations
  • Environment International (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • edoc (University of Basel) (acceptedVersion)
  • Lirias (submittedVersion, other-oa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • edoc (University of Basel)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Vitamin D Research Studies
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
vitamin D deficiency, air pollution, particulate matter, environmental chemicals, smoking, endocrine disruptors, heavy metals, vitamin D metabolism, cutaneous vitamin D synthesis, UV-B radiation, cytochrome P450, renal tubular dysfunction, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, calcium homeostasis, thyroid hormones, parathyroid hormone, skin aging
MeSH terms
Air Pollution, Environmental Exposure, Humans, Smoking, Vitamin D, Vitamin D Deficiency, Particulate Matter

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