**1. Introduction**

Bisphenol A [4,4′‐(propane‐2,2‐diyl)diphenol] (abbreviated as BPA) is a synthetic xenoestro‐ genic chemical and endocrine disruptor [1–3] widely used in dentistry, food packaging and as lacquers to coat food cans, bottle‐tops and water pipes since the 1960s. It is a most common plasticizer that is used widely to produce epoxy resin and polycarbonate plastics. It was first synthesized by Dianin in 1891 and was investigated for potential commercial use in the 1930s during a search for synthetic estrogens. BPA enters the living system inconspicuously through various routes, particularly through food and water contamination, and creates multitude of imperilments at cellular, molecular and genetic level. The EC50 and LC50 values of BPA range

from 1.0 to 10 mg/L (Environment Canada 2008), and BPA is declared as 'moderately toxic' and 'toxic' to aquatic biota by the European Commission and the United States Environmental Protection Agency (US EPA), respectively [4], Commission of the European Communities 1996]. Moreover, environmentally relevant concentrations (12 mg/L or lower) of BPA were also found to be harmful as far as wildlife is concerned [5]. BPA exerts its effect through direct binding to estrogen receptor (ER) in a wide range of species that includes invertebrates, fish, amphibians, reptiles, birds and mammals [6]. BPA binds both ERα and ERβ receptors, with approximately 10‐fold higher affinity to ERβ [7].

The toxicokinetics of BPA exposure reveal that after oral administration in human, BPA is metabolized rapidly in the intestine and liver. BPA is not completely metabolized via Phase I reactions, but it is rapidly conjugated with glucuronic acid (Phase II metabolism) to pro‐ duce non‐active BPA‐glucuronide in the gut wall and liver. Little amount of BPA also reacts with sulphate to form BPA‐sulphate compound. The formation of BPA conjugates with other chemical moieties is a detoxification process [8, 9]. The BPA conjugates formed in the liver reach the kidney through blood circulation and then excreted in the urine with terminal half‐ lives of less than 6 hours [10, 11]. According to a declaration made in 2010 by U.S. Food and Drug Administration, exposure to BPA is alarming because of possible health hazards it exerts on brain, behaviour and prostate gland of foetuses, infants and children. The European Food Safety Authority (EFSA) reviewed new scientific information on BPA in the years 2008, 2009, 2010, 2011 and 2015, concluding on each occasion the known level of exposure to BPA to be hazardous. In February 2016, France announced that it intends to propose BPA as a REACH Regulation candidate substance of very high concern (SVHC).

Owing to difficulty in doing research on human subjects, researchers prefer to use model organisms to test the toxic effect of xenobiotic agents in living system. This approach is also popular in the research on BPA as the agent is ubiquitously present in our 'plastic wrapped world' and no perfect control subject could be obtained in natural environment. Several model organisms from different taxa are in use for studying the effects of BPA on their life history, morphological traits, reproductive functioning, neural functioning and behaviour. The outcome of these studies helps to anticipate the probable adversity that BPA inflicts in human body. Keeping all these factors in mind, a critical review on latest research works is presented here to understand the deleterious effects of BPA exposure on different vertebrate and invertebrate model organisms that could facilitate the understanding of human health hazards due to exposure to this xenoestrogen and endocrine disruptor BPA.
