Bone and joints
One of the main effects of cadmium poisoning is weak and brittle bones. The bones become soft (osteomalacia), lose bone mineral density (osteoporosis), and become weaker. This results in joint and back pain, and increases the risk of fractures. Spinal and leg pain is common, and a waddling gait often develops due to bone deformities caused by the long-term cadmium exposure. The pain eventually becomes debilitating, with fractures becoming more common as the bone weakens. Permanent deformation in bones can occur. In extreme cases of cadmium poisoning, more body weight causes a fracture. Renal
The kidney damage inflicted by cadmium poisoning is irreversible. The kidneys can shrink up to 30 percent. The kidneys lose their function to remove acids from the blood in proximal renal tubular dysfunction. The proximal renal tubular dysfunction causes hypophosphatemia, leading to muscle weakness and sometimes coma. Hyperchloremia also occurs. Kidney dysfunction also causes gout, a form of arthritis due to the accumulation of uric acid crystals in the joints because of high acidity of the blood (hyperuricemia). Cadmium exposure is also associated with the development of kidney stones. Sources of exposure
Smoking is a significant source of cadmium exposure. Even small amounts of cadmium from smoking are highly toxic to humans, as the lungs absorb cadmium more efficiently than the stomach. Cadmium is emitted to the electronic cigarette (EC) aerosol but, on currently available data, the  lifetime  cancer  risk (LCR) calculated doesn’t  exceed the acceptable risk limit.
Depending on the location of the exostoses they cause numerous complications such as compression of the spinal cord, asymmetric growth of the limbs and reduced mobility.Langer–Giedion syndrome initially causes joint hypermobility. This progresses to joint stiffness later in life when osteochondromas begin to develop, typically between infancy and mid-childhood, which decreases mobility. Hip dysplasia may be present, usually developing in early adulthood although it can occur in infancy or childhood. Skin, hair, sweat glands and nails
Ectodermal dysplasia is a key feature of Langer–Giedion syndrome.The majority of individuals with Langer–Giedion syndrome have sparse scalp hair; this is particularly severe in males, who often experience alopecia shortly after puberty. Despite this the eyebrows may be unusually thick. Cause
The syndrome occurs when a small piece of chromosome 8s long arm, which contains a number of genes, is missing. The loss of these genes is responsible for some of the overall characteristics of Langer–Giedion syndrome.The missing portion of the chromosome is 8q23.2–q24.1. This region includes the genes TRPS1 and EXT1. Diagnosis
Diagnosis is based on clinical findings and can be confirmed by cytogenetic testing, when the deletion is in an average of 5 Mb (millions of base pairs). Nowadays, it is a common practice to run an aCGH (array chromosome hybridization genome) study on peripheral blood of the patient, in order to delineate the extent of the loss of the genomic area, and the deleted genes. Treatment
While no genetic syndrome is capable of being cured, treatments are available for some symptoms. External fixators have been used for limbic and facial reconstructions.