Air pollution, environmental chemicals, and smoking may trigger vitamin D deficiency: Evidence and potential mechanisms
Environment International, online 30 Nov 2018 https://doi.org/10.1016/j.envint.2018.11.052t
- Immune system is suppressed by many things (many of which consume vitamin D)
- Vitamin D reduced so low that Victorian age diseases are returning
Air Pollution reduces Vitamin D
- Traffic pollution increases asthma unless supplement with Vitamin D (mice) June 2018
- Vitamin D level: 27 ng if low pollution, 12 ng if high pollution (Delhi children) – June 2018
- Air Pollution 2000-2012 nice interactive maps
- Fewer pre-term births after pollution reduction (vitamin D not mentioned) April 2014
- Household chemicals found to be the source of half of urban pollution (and thus decreased urban vitamin D) – Feb 2018
- Higher air pollution associated with 7 ng lower vitamin D levels – Aug 2013
- Cadmium liver problem 5 X less likely when vitamin D is greater than 40 ng – April 2018
- Lead in breastmilk reduced vitamin D levels in blood by a third (in rats) – Feb 2018
- A good Vitamin D Receptor (or perhaps more vitamin D) protects against lead during pregnancy
- Pesticides increase risk of Cancers, Alz, ALS, Asthma, ADHD, etc. (all related to low vitamin D) – Oct 2016
- DDT 3.8 X more prevalent with Alzheimer disease (no mention that DDT decreases vitamin D) – Jan 2014
- DDT and other pesticides decrease vitamin D
- Plastics, BPA, PCB and Vitamin D deficiency
- PCBs increased the chance of being Vitamin D deficient by 3 percent – May 2013
- Investigation on Roundup - glyphosate at VitaminDWiki apparently not mention by study on this page
Download the PDF from VitaminDWiki
EDC = Endocrine-disrupting chemicals
Possible Smoking pathways
Fig. 4. Potential mechanisms related to the disruption of VDES by tobacco smoke.
The positive and negative signs on the end of the arrows imply increasing and decreasing the targets, respectively.
Red arrows originated from the cigarette result in decreasing serum 25(OH)D and 1,25(OH)2D levels, VD intake from diet, and the cutaneous production of VD. These four items determine the VD level of individuals. From a systematic point of view, cigarette smoke leads to depression of VD levels in humans. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
- Air pollution may lead to vitamin D deficiency (VDD) directly or indirectly.
- Heavy metals may lead to VDD by increasing renal tubular dysfunction and downregulating the transcription of CYPs.
- Endocrine-disrupting chemicals may directly inhibit the activity and expression of CYPs and through indirect pathways.
- Smoking causes VDD through several pathways.
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.