**3.5 Others**

Exposure to EDCs has been reported to be associated with increased incidence of cardiovascular, respiratory, liver, kidney, neurological/psychiatric, skin, and immunological disorders [2–4, 10, 13, 16, 24, 42–44].

Skin is a body barrier providing protection from environmental physical and chemical harm. Several EDCs (e.g., dioxins, phthalates, parabens, and arsenic) can act directly on different skin cells (e.g., keratinocytes, sebocytes, melanocytes, stem cells, and fibroblasts) and cause a variety of skin disorders such as chloracne, hyperpigmentation, allergic contact dermatitis, aging, and cancer (**Figure 8**) [44].

**Figure 8.** *EDCs can cause a variety of skin disorders.*

#### **3.6 Timing of exposure to EDCs**

The timing of exposure to EDCs plays an important role for the health consequences of EDCs.

Pregnancy is a sensitive window for EDCs exposure. Pregnant women are exposed to numerous EDCs (e.g., bisphenol A, phthalates, parabens, and flame retardants) which can cross the placenta and affect the fetus. The developing fetus and neonate are more sensitive than adults to perturbation by EDCs (**Figure 9**) [3, 4, 9, 10, 14, 16, 17, 19, 25–28, 37–39, 41, 43, 46]. There is a higher sensitivity in fetus and neonate due to rapid cell division and differentiation, lack of protective mechanisms (e.g., DNA repair), competent immune system, or mature blood/ brain barrier, and increased metabolic rates. During fetal development, different organ systems begin to develop at different time periods. Therefore, the susceptibility to EDC exposure and health consequences depends on the critical period for a given target organ system. The prenatal damage can cause adverse consequences later in life (developmental origins of adult disease). Effects on early development are of special concern as these effects are often irreversible. Oxidative stress caused by EDCs can be the mediator of several adverse health outcomes (e.g., obesity, diabetes, and cardiovascular disease in adulthood) [16, 19, 46]. With EDCs, there is also a possibility of damage to future generations (transgenerational inheritance) [10, 16, 17, 27, 28].

**375**

**Figure 10.**

*Human Health Consequences of Endocrine-Disrupting Chemicals*

*DOI: http://dx.doi.org/10.5772/intechopen.94955*

**3.7 Dose and duration of exposure to EDCs**

nated diphenyl ethers in the USA [47].

*EDCs can severely impact the developing fetus.*

**Figure 9.**

**3.8 Gender effect of exposure to EDCs**

*Gender may influence the health consequences of EDCs.*

girls versus increase in internalizing behavior in boys).

The intensity of exposure to EDCs varies between the United States of America (USA) and the EU because of differences in regulations. For example, EDC exposure is much higher for organophosphate pesticides in the EU and for polybromi-

Humans are at the top of food chain. They may store large doses of multiple EDCs according to the process of bioaccumulation and bioamplification, generating effects with unknown consequences [12]. No safe dose of EDC exposure can be established. Information on chronic low-dose exposure to EDCs is relatively limited.

Based on epidemiological studies, gender may play a role on the impact of EDCs

(**Figure 10**) [12, 16, 42]. EDCs exert sexually dimorphic effects in metabolism regulation through interactions with sex hormone receptors. Bisphenol A appears to have specific effects on behavior of both sexes (increase in externalizing behavior in

**Figure 9.** *EDCs can severely impact the developing fetus.*

*Environmental Issues and Sustainable Development*

immunological disorders [2–4, 10, 13, 16, 24, 42–44].

Exposure to EDCs has been reported to be associated with increased incidence of cardiovascular, respiratory, liver, kidney, neurological/psychiatric, skin, and

Skin is a body barrier providing protection from environmental physical and chemical harm. Several EDCs (e.g., dioxins, phthalates, parabens, and arsenic) can act directly on different skin cells (e.g., keratinocytes, sebocytes, melanocytes, stem cells, and fibroblasts) and cause a variety of skin disorders such as chloracne, hyperpigmentation, allergic contact dermatitis, aging, and cancer

The timing of exposure to EDCs plays an important role for the health conse-

Pregnancy is a sensitive window for EDCs exposure. Pregnant women are exposed to numerous EDCs (e.g., bisphenol A, phthalates, parabens, and flame retardants) which can cross the placenta and affect the fetus. The developing fetus and neonate are more sensitive than adults to perturbation by EDCs (**Figure 9**) [3, 4, 9, 10, 14, 16, 17, 19, 25–28, 37–39, 41, 43, 46]. There is a higher sensitivity in fetus and neonate due to rapid cell division and differentiation, lack of protective mechanisms (e.g., DNA repair), competent immune system, or mature blood/ brain barrier, and increased metabolic rates. During fetal development, different organ systems begin to develop at different time periods. Therefore, the susceptibility to EDC exposure and health consequences depends on the critical period for a given target organ system. The prenatal damage can cause adverse consequences later in life (developmental origins of adult disease). Effects on early development are of special concern as these effects are often irreversible. Oxidative stress caused by EDCs can be the mediator of several adverse health outcomes (e.g., obesity, diabetes, and cardiovascular disease in adulthood) [16, 19, 46]. With EDCs, there is also a possibility of damage to future generations (transgenerational inheritance)

**3.5 Others**

(**Figure 8**) [44].

**3.6 Timing of exposure to EDCs**

*EDCs can cause a variety of skin disorders.*

quences of EDCs.

**Figure 8.**

**374**

[10, 16, 17, 27, 28].
