PMID- 23509204
OWN - NLM
STAT- MEDLINE
DCOM- 20130722
LR  - 20130424
IS  - 0048-7554 (Print)
IS  - 0048-7554 (Linking)
VI  - 28
IP  - 1
DP  - 2013
TI  - Lipophilic chemical exposure as a cause of type 2 diabetes (T2D).
PG  - 9-20
LID - 10.1515/reveh-2012-0031 [doi]
AB  - The prevalence of type 2 diabetes (T2D) is increasing worldwide in pandemic-like 
      numbers. It is considered, at least in part, to be an environmental illness. 
      Recent research has shown that diabetes can be caused by exposure to persistent 
      organic pollutants (POPs), exudates from common plastics, air pollution, primary 
      and secondary tobacco smoke, and some pharmaceuticals. These chemicals vary 
      widely in structure, chemical properties, and composition and are not currently 
      believed to induce a similar effect. A unifying explanation for the induction of 
      T2D by this diversified group of chemicals is proposed here. These toxicants have 
      one thing in common. All are lipophilic species that permeate lipophilic body 
      membranes, thereby promoting the absorption of toxic hydrophilic species that 
      would otherwise not penetrate lipophilic membranes. It is further proposed that 
      exposure to the lipophilic and hydrophilic species need not occur simultaneously 
      but can occur sequentially, with the lipophile absorbed first and retained in 
      body serum, followed by a subsequent exposure to the hydrophile. The lipophilic 
      chemical can be one of the POPs (including dioxins, furans, polychlorinated 
      biphenyls, polybrominated biphenyls, polybrominated diphenyl ethers, or 
      organochlorine pesticides); a more rapidly metabolized or eliminated species 
      including plastic exudates like phthalate esters and bisphenol A; air pollutants 
      and tobacco smoke components including aliphatic, aromatic, or polynuclear 
      aromatic hydrocarbons; or pharmaceuticals like some statins and second-generation 
      antipsychotic drugs. This hypothesis suggests that the T2D pandemic as well as 
      the rapid increase of other environmental disease prevalence is, at least in 
      part, due to sequential exposure to levels of lipophilic and hydrophilic 
      environmental pollutants that are much lower than those currently believed to be 
      toxic. As a consequence of this hypothesis, the allowable levels of exposure to 
      these pollutants should be dramatically lowered.
FAU - Zeliger, Harold I
AU  - Zeliger HI
AD  - Toxicological and Environmental Research, West Charlton, NY 12010, USA. 
      hiz@zeliger.com
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Rev Environ Health
JT  - Reviews on environmental health
JID - 0425754
RN  - 0 (Environmental Pollutants)
SB  - IM
MH  - Adipose Tissue/*drug effects
MH  - Cluster Analysis
MH  - Diabetes Mellitus, Type 2/*chemically induced
MH  - Environmental Pollutants/*toxicity
MH  - Humans
EDAT- 2013/03/20 06:00
MHDA- 2013/07/23 06:00
CRDT- 2013/03/20 06:00
PHST- 2012/11/13 00:00 [received]
PHST- 2013/01/02 00:00 [accepted]
PHST- 2013/03/20 06:00 [entrez]
PHST- 2013/03/20 06:00 [pubmed]
PHST- 2013/07/23 06:00 [medline]
AID - /j/reveh.ahead-of-print/reveh-2012-0031/reveh-2012-0031.xml [pii]
AID - 10.1515/reveh-2012-0031 [doi]
PST - ppublish
SO  - Rev Environ Health. 2013;28(1):9-20. doi: 10.1515/reveh-2012-0031.