crops. Cadmium concentrated in the crops, and local women began to experience
pain in bones and joints, eventually becoming so excruciating that they were
bedridden. Cadmium interfered with calcium metabolism, leading to reduction in
calcium levels and thus reduced density and strength of bones, often causing the
weakened bones to break (Watanabe et al. 2004).
Symptoms and signs of “itai-itai” disease include:
• Severe osteoporosis and osteomalacia with simultaneous severe renal
dysfunction.
• Normochromic anemia and low blood pressure sometimes also occur (Alfvén
et al. 2002; Nogawa et al. 2004).
4.1.3 Cancer Risk
Cd is a multi-site carcinogen in both rodents and humans and has been classified as a
Class B1 carcinogen by the International Agency for Research on Cancer and the US
Environmental Protection Agency (Waalkes et al. 2000; Huff et al. 2007). Many
studies have found a linkage between occupational exposure to cadmium and
pulmonary cancer (Nawrot et al. 2006), as well as prostate (Zeng et al. 2004),
renal (Pesch et al. 2000), liver and stomach (Waalkes and Misra 1996), and urinary
bladder cancer (Kellen et al. 2007). Waalkes (2003) reported increased risks of lung
cancer in workers exposed to Cd by inhalation. In another study a significant trend
for lung cancer risk was found only by the combined exposure to arsenic and
cadmium suggesting that cadmium is carcinogenic only in the presence of concomitant exposure to arsenic. Cd exposure in the industry has also been linked to prostate
and renal cancer, but this linkage is much weaker than that for lung cancer. In a
Cd-polluted region in China, an association between urinary Cd and raised serum
concentration of prostate-specific antigen has been found suggesting a possible
implication of Cd in prostate carcinogenesis (Zeng et al. 2004). Garcia-Morales
et al. (1994) observed an association between cadmium exposure and human breast
cancer, and it has been suggested that the effects of cadmium are mediated by the
estrogen receptor independent of estradiol. However, the mechanism of Cd carcinogenesis remains largely unknown. Since the metal is not strongly genotoxic and does
not cause direct genetic damage, epigenetic mechanisms and/or indirect genotoxic
mechanisms such as a blockage of apoptosis, alterations in cell signaling, or inhibition of DNA repair might be involved (Waalkes 2003).
4.1.4 Respiratory Effects
There have also been studies examining the role of cadmium in the development of
chronic obstructive pulmonary disease (COPD) in smokers. Inhalation causes respiratory stress and injures the respiratory tract (ATSDR 1999). Emphysema, anosmia,
and chronic rhinitis have been linked to high cadmium concentrations in polluted air.
15 Cadmium as an Environmental Pollutant: Ecotoxicological Effects, Health. . .
365
pain in bones and joints, eventually becoming so excruciating that they were
bedridden. Cadmium interfered with calcium metabolism, leading to reduction in
calcium levels and thus reduced density and strength of bones, often causing the
weakened bones to break (Watanabe et al. 2004).
Symptoms and signs of “itai-itai” disease include:
• Severe osteoporosis and osteomalacia with simultaneous severe renal
dysfunction.
• Normochromic anemia and low blood pressure sometimes also occur (Alfvén
et al. 2002; Nogawa et al. 2004).
4.1.3 Cancer Risk
Cd is a multi-site carcinogen in both rodents and humans and has been classified as a
Class B1 carcinogen by the International Agency for Research on Cancer and the US
Environmental Protection Agency (Waalkes et al. 2000; Huff et al. 2007). Many
studies have found a linkage between occupational exposure to cadmium and
pulmonary cancer (Nawrot et al. 2006), as well as prostate (Zeng et al. 2004),
renal (Pesch et al. 2000), liver and stomach (Waalkes and Misra 1996), and urinary
bladder cancer (Kellen et al. 2007). Waalkes (2003) reported increased risks of lung
cancer in workers exposed to Cd by inhalation. In another study a significant trend
for lung cancer risk was found only by the combined exposure to arsenic and
cadmium suggesting that cadmium is carcinogenic only in the presence of concomitant exposure to arsenic. Cd exposure in the industry has also been linked to prostate
and renal cancer, but this linkage is much weaker than that for lung cancer. In a
Cd-polluted region in China, an association between urinary Cd and raised serum
concentration of prostate-specific antigen has been found suggesting a possible
implication of Cd in prostate carcinogenesis (Zeng et al. 2004). Garcia-Morales
et al. (1994) observed an association between cadmium exposure and human breast
cancer, and it has been suggested that the effects of cadmium are mediated by the
estrogen receptor independent of estradiol. However, the mechanism of Cd carcinogenesis remains largely unknown. Since the metal is not strongly genotoxic and does
not cause direct genetic damage, epigenetic mechanisms and/or indirect genotoxic
mechanisms such as a blockage of apoptosis, alterations in cell signaling, or inhibition of DNA repair might be involved (Waalkes 2003).
4.1.4 Respiratory Effects
There have also been studies examining the role of cadmium in the development of
chronic obstructive pulmonary disease (COPD) in smokers. Inhalation causes respiratory stress and injures the respiratory tract (ATSDR 1999). Emphysema, anosmia,
and chronic rhinitis have been linked to high cadmium concentrations in polluted air.
15 Cadmium as an Environmental Pollutant: Ecotoxicological Effects, Health. . .
365