What are the signs, symptoms, and long-term complications of acute and chronic cadmium exposure?

1. Acute exposure: early signs that mimic the flu but can hide lung injury

Initial symptoms from a short, high‑level inhalation of cadmium often resemble metal fume fever or influenza—fever, chills, muscle pain, headache, malaise and upper respiratory irritation such as cough and sore throat—sometimes with a metallic taste; these manifestations may be delayed for hours after exposure ^{[1] Cadmiumpoisoning" target="blank" rel="noopener noreferrer">[7] [3]}. Gastrointestinal irritation and acute gastritis can occur when cadmium is ingested in significant amounts—classical scenarios include acidic foods stored in cadmium‑glazed containers—producing nausea and epigastric pain ^[2].

2. Acute complications: when a flu‑like illness becomes life‑threatening lung disease

In more intense inhalational exposures the initial flu‑like picture can progress over hours to days to acute chemical pneumonitis, pulmonary edema, bronchitis, respiratory failure and death; reported mortality after severe acute exposures is substantial and survivors can be left with long‑term impaired lung function or progressive pulmonary fibrosis ^{[2] [3] [8]}. Occupational case reports—welders and people disturbing cadmium‑containing paints or solders—document both fatal acute pulmonary edema and protracted respiratory disability in survivors ^{[9] [3]}.

3. Chronic exposure: stealth accumulation and early clinical clues

Cadmium accumulates in the body over years, concentrating especially in renal cortex and lung and persisting long after exposure ends; early biomarkers of chronic exposure include raised urinary cadmium and tubular proteinuria (β2‑microglobulin, α1‑microglobulin) that may appear at relatively low urinary cadmium concentrations ^{[4] [5]}. Chronic respiratory effects include chronic rhinitis, anosmia from olfactory epithelial damage, bronchitis and increased susceptibility to infections and emphysema—findings that are reinforced in smokers where inhaled cadmium contributes to smoking‑related lung disease ^{[4] [10]}.

4. Long‑term complications beyond the lungs: kidneys, bones, cancer and cardiovascular disease

The dominant chronic lesion is toxic nephropathy: progressive renal tubular dysfunction with proteinuria, glycosuria, aminoaciduria, and ultimately reduced glomerular filtration and renal failure in severe cases, and urinary biomarkers correlate with stages of injury ^{[4] [5] [11]}. Skeletal disease ranges from calcium wasting to osteomalacia and severe osteoporosis—exemplified by Japan’s itai‑itai disease—linked to cadmium‑induced renal loss of calcium and phosphate ^{[5] [4]}. Epidemiologic and toxicologic evidence links cadmium exposure to increased incidence of several cancers—notably lung and possibly prostate and other sites—while mechanistic and population studies also suggest cardiovascular effects including hypertension, endothelial damage, atherogenesis and peripheral arterial disease ^{[9] [11] [6]}.

5. Diagnosis, management and areas of uncertainty

Diagnosis of acute exposure relies on clinical presentation and cadmium blood levels, whereas chronic burden is best assessed with urinary cadmium and renal biomarkers such as β2‑microglobulin and N‑acetyl‑β‑glucosaminidase; imaging and pulmonary function testing assess organ damage ^{[11] [4]}. There is no single universally accepted antidote; management focuses on removing exposure, supportive care for pulmonary or renal failure, and monitoring—some chelation strategies have been discussed in literature but evidence, especially for chronic removal and renal outcomes, remains limited and context‑dependent ^{[7] [11]}. Evidence gaps and confounders exist in cancer attribution and precise exposure‑response thresholds for many endpoints, and many authoritative sources caution that epidemiologic links are influenced by smoking and occupational co‑exposures, underscoring limits in attributing causality at low environmental levels ^{[1] [8] [6]}.