This figure represents the number of cars, trucks (light, medium and heavy duty), and buses, but does not include off-road vehicles or heavy construction equipment. The world vehicle population passed the 500 million-unit mark in 1986, from 250 million motor vehicles in 1970. Between 1950 and 1970, the vehicle population doubled roughly every 10 years. Navigant Consulting forecasts that the global stock of light-duty motor vehicles will reach 2 billion units in 2035.Global vehicle ownership in 2010 was 148 vehicles in operation per 1000 people, a ratio of 1:6.75 vehicles to people, slightly down from 150 vehicles per 1000 people in 2009, a rate of 1:6.63 vehicles to people. The global rate of motorization increased in 2013 to 174 vehicles per 1000 people. In developing countries vehicle ownership rates rarely exceed 200 cars per 1,000 population.The following table summarizes the evolution of motor vehicle registrations in the world from 1960 to 2019:

Alternative fuels and vehicle technology adoption

Since the early 2000s, the number of alternative fuel vehicles has been increasing driven by the interest of several governments to promote their widespread adoption through public subsidies and other non-financial incentives.
The disorder exhibits a highly variable penetrance among family members. Hereditary fibrinogen Aα-Chain amyloidosis shows variable penetrance among family members, a distinctive histological appearance, proteinuria, progressive renal impairment, and markedly better survival rates than other forms of systemic renal amyloidosis. Treatment
Treatment of hereditary fibrinogen Aα-Chain amyloidosis has relied on chronic maintenance hemodialysis and, where possible, kidney transplantation. While recurrence of amyloidosis in the transplanted kidney occurs and is to be expected, transplant survival rates for this form of amyloidosis are significantly better than those for transplants in other forms of systemic renal amyloidosis. Relatively healthy individuals with hereditary fibrinogen Aα-Chain-related renal amyloidosis may be considered for kidney and liver bi-transplantation with the expectation that survival of the transplanted kidney will be prolonged by replacing the fibrinogen Aα-Chain-producing liver with a non-diseased donor liver. Acquired dysfibrinogenemia
Presentation
Acquired dysfibrinogenemia commonly present with signs, symptoms, and/or prior diagnoses of the underlying causative disease or drug intake in an individual with an otherwise unexplained bleeding tendency or episode. Bleeding appears to be more prominent in acquired compared to congenital dysfibrinogenemia; pathological thrombosis, while potentially occurring in these individuals as a complication of their underlying disease, is an uncommon feature of the acquired disorder. Pathophysiology
Acquired dysfibrinogenemia occurs as a known or presumed consequence of an underlying disease which directly or indirectly interferes with the clotting function of fibrinogen. Individuals with acquired dysfibrinogenemias have a greater tendency for bleeding complications than those with congenital fibrinogenemia.